# Inflammatory Breast Diseases during Lactation:  Health Effects on the Newborn—A Literature Review

Authors: Achim Wöckel; Michael Abou-Dakn; Anna Beggel; Petra Arck
Journal: Mediators of Inflammation
 (2008)

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## Abstract

Breastfeeding-associated inflammatory breast diseases appear especially during the first twelve  weeks postpartum and are the most common reason for early cessation of breastfeeding. It also becomes increasingly evident that these inflammatory mammary diseases are triggered or perpetuated in a large part by psychosocial stress. Immunological  processes taking place during this cascade in the mammary gland and consequences for the breastfeed newborn are mostly yet unknown. This review summarizes insights from studies on modulation of cytokine levels in breast milk during inflammatory processes like milk stasis  and mastitis systematically. It also gives an overview on possible pathological effects, which these cytokine changes in the breast milk might have on the newborn.


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## Body

## 1. Introduction

### 1.1. Milk Stasis and Mastitis

The WHO suggests a six-month
period of breastfeeding to all  breastfeeding mothers [1]. Evidence-based advantages for mother and
child result especially  when children in this time are fed exclusively without
any additional breast milk supplements [2]. Only 50% of women worldwide
reach this goal [3]. The remaining mothers very often add supplements or cease
breastfeeding completely because they suffer from inflammatory breast diseases
like milk stasis or puerperal mastitis [4].These breastfeeding-associated
inflammatory breast diseases appear especially during the first twelve weeks
postpartum and are the most common reason for an early cessation of
breastfeeding [5]. Changes develop like a cascade [4–6]: first
little erosions caused by  the suckling of the infant lead to severe nipple and areolar pain. Pain anticipates an undisturbed breastfeeding relationship and leads to an
insufficient emptying of the breast by the newborn. An insufficient emptying of the breast can
subsequently lead to a stasis in the mammary alveoli. This milk stasis augments
pain and opens intercellular junctions between the milk duct epithelial cells
caused by a rise of intraductal pressure. Breast milk, then moving into the
connective tissue, leads to a primary a sterile inflammation, generally followed by a
secondary bacterial infection. In the worst cases, this results in a puerperal
mammary abscess, which has to be surgically treated.Immune mediators such as
cell subsets or cytokines involved in this perpetuating inflammation in the
mammary gland in humans are mostly unknown.In veterinary medicine, a number of scientists work on the subject
focussing on bovine mastitis in experimental studies, since bovine mastitis
causes enormous economic damage in the dairy industry [7], and hence,
the dairy industry has a vast interest in the development of analytical methods
to identify animals at risk when symptoms are still inapparent. The goal of
these research endeavors is to identify early risk markers, that is in milk or
maternal serum. In this context, the somatic cell count (SCC/mL), bacterial
count (colony-forming units [CFUs]/mL), ratio of milk phagocytes (mononuclear
[Mphi] plus polymorphonuclear [PMN] cells) to lymphocytes (P/L index), and
ratio of PMN to Mphi cells (PMN/Mphi index) and also the measurement of
cytokines in milk could be used to identificate the inflammatory reactions in
the mammary tissue [8]. Immunomodulating agents are also normally present in human milk in
physiologically relevant quantities but there is a wide range of concentrations
of different cytokines at each time during the first 12 weeks of lactation: IL-1: 15-400 pg/mL; IL-6: 15-1032 pg/mL; TNF-alpha:
15-2933 pg/mL; Prostaglandin E2: 10-9966 pg/mL; TGF-beta1: 43-7108 pg/mL;
TGF-beta2: 208-57935 pg/mL [9].


### 1.2. Diseases of the Breast During Lactation and Stress

It is generally believed
that inflammatory breastfeeding-associated mammary diseases may be triggered or
aggravated by psychosocial stress, as observed for example in veterinary medicine. Here, exposure to experimental stressors
such as regrouping and relocation resulted into mastitis in animals, as
described for lactating ewes [10]. In humans, clinical observations
reveal similar correlations: mothers with breastfeeding-associated diseases
(milk stasis and mastitis) report an increased stress perception, that is due
to events in their social network in the weeks prior to the clinical symptoms [11].
Recent studies performed by the authors further support the alleged causality
of stress perception and puerperal diseases in humans [12].What
are the possible pathophysiological mechanisms of stress-dependent breast
diseases during lactation? The increased secretion of catecholamines in
stressed mothers impairs the release and access of oxytocin to the mammary
gland and the action of oxytocin on the secretory epithelium [13]. The release of oxytocin in response to stressful stimuli may reduce
the availibility of this hormone at the
suckling reflex. Stress  also leads to higher levels of prolactine and thus to
an increased synthesis of breast
milk. The reduced release or impaired action of oxytocin and the
coexistent higher proposal of breast milk cause an incomplete emptying of the alveoli and
galactophorus ducts and lead
to milk stasis.Stressfull
events may also cause immune supression in the mammary tissue. T-lymphocytes have
regulatory functions or act directly on foreign antigens because of producing
cytokines. T-lymphocytes are strongly involved in the defense against bacterial
invasion during mastitis [14]. These cells are
uniquely sensitive to soluble modulating factors, so it is likely that the
neuroendocrine response in stress elaborates hormones and peptides that may
have a major impact on cell mediated immunity [15]. The
increase in maternal stress perception has recently been shown to cause a
priming of the maternal immune system towards a proinflammatory, Th1-cytokine
response (IL-1, IL-6, TNF-a, INF-y) instead of anti-inflammatory Th2-cytokines
(IL-4, IL-5, IL-9 and IL-13) in the mammary tissue [12].At birth the immune
system of the neonate is primed towards a Th2 dominance. Within the first 2
years of life, the immune system is activated, probably via childhood
infections, leading to a naturally occurring shift from Th2 to Th1 immunity.
Intestinal mucosa is also premature in the first two years. Thus higher
concentrations of proinflammatory Th-1-cytokines in the breast
milk may
lead to local and systemic immunological effects of the newborn [16].


### 1.3. Modified Cytokine
Patterns of the Breast Milk and Their Effects on the
Child

Maternal stress
perception is likely intimately linked to stress reactions of the newborn.
Published data indicate that the offspring may develop somatic diseases [17], well described
for atopic dermatitis, bronchitis, and allergic
diseases in response to maternal stress perception [16, 18]. Most of
these studies focus on imprinting such as maternal stress perception
programming the child in utero,
which is generally referred to as the fetal programming hypothesis.
Surprisingly, to date, the period of lactation has received very little
attention in this context. Here, it has been described that a long period of
lactation minimizes the risk for infection of the offspring due to high levels
of IgA in breast milk, which may protect the offspring from infectious diseases [19].
However, it still remains to be elucidated if and how maternal stress
perception affects immune markers in the breast milk and whether such
alterations may have consequences for the child’s well being. Given the yet
unexplained dramatic increase of chronic inflammatory diseases in children over
the past 5 decades [20], the identification of a vicious cycle between
stress perception, impaired breastfeeding/nutrition of the offspring and the
onset of chronic diseases is urgently required and it is the aim of the present
review to foster future research in this direction.If a major part of breast diseases, as proven in our own surveys, is caused by stress and at
the same time the prevalence of these diseases is relatively high [12],
a change in the constituents of breast milk would be imaginable. One possibility
is a change in the cytokine profile in breast milk, which then might lead to
diseases in the child (Figure 1). Further, recent studies predominately arising
from rodents have elegantly shown that the epigenome of the developing fetus is
sensitive to maternal nutrition, exposure to environmental toxins as well as to
psychological stress [21]. It is postulated that exposure of the young
pup to social behavior, such as maternal care, could affect the epigenome.
Epigenetic alterations, which could have similar consequences as genetic
polymorphisms, have been shown to arise from variations of maternal behavior
and may account for differences in human behavior and possibly vulnerability to
diseases later in life of the offspring. Hence,
impaired breastfeeding could affect the growing offspring in a number of ways, that
is via an altered immune cocktail in the breast milk. But also impaired
maternal caring behavior due to discontinuation of breastfeeding may lead to
effects on the psychological development and thus on the immune system of the
newborn, because breastfeeding seems to be also very important for emotional
bonding [22].Figure 1
Vicious cycle
of increased maternal stress perception,
inflammatory breast diseases, and diseases of the newborn transmitted by
changes in the cytokine pattern in breast milk.The aim of this systematic review was to show detectable changes of
cytokines in breast milk during inflammatory processes of mammary tissue like
mastitis and possible pathological effects of these mediators on the newborn
caused by breastfeeding.


## 1.1. Milk Stasis and Mastitis

The WHO suggests a six-month
period of breastfeeding to all  breastfeeding mothers [1]. Evidence-based advantages for mother and
child result especially  when children in this time are fed exclusively without
any additional breast milk supplements [2]. Only 50% of women worldwide
reach this goal [3]. The remaining mothers very often add supplements or cease
breastfeeding completely because they suffer from inflammatory breast diseases
like milk stasis or puerperal mastitis [4].These breastfeeding-associated
inflammatory breast diseases appear especially during the first twelve weeks
postpartum and are the most common reason for an early cessation of
breastfeeding [5]. Changes develop like a cascade [4–6]: first
little erosions caused by  the suckling of the infant lead to severe nipple and areolar pain. Pain anticipates an undisturbed breastfeeding relationship and leads to an
insufficient emptying of the breast by the newborn. An insufficient emptying of the breast can
subsequently lead to a stasis in the mammary alveoli. This milk stasis augments
pain and opens intercellular junctions between the milk duct epithelial cells
caused by a rise of intraductal pressure. Breast milk, then moving into the
connective tissue, leads to a primary a sterile inflammation, generally followed by a
secondary bacterial infection. In the worst cases, this results in a puerperal
mammary abscess, which has to be surgically treated.Immune mediators such as
cell subsets or cytokines involved in this perpetuating inflammation in the
mammary gland in humans are mostly unknown.In veterinary medicine, a number of scientists work on the subject
focussing on bovine mastitis in experimental studies, since bovine mastitis
causes enormous economic damage in the dairy industry [7], and hence,
the dairy industry has a vast interest in the development of analytical methods
to identify animals at risk when symptoms are still inapparent. The goal of
these research endeavors is to identify early risk markers, that is in milk or
maternal serum. In this context, the somatic cell count (SCC/mL), bacterial
count (colony-forming units [CFUs]/mL), ratio of milk phagocytes (mononuclear
[Mphi] plus polymorphonuclear [PMN] cells) to lymphocytes (P/L index), and
ratio of PMN to Mphi cells (PMN/Mphi index) and also the measurement of
cytokines in milk could be used to identificate the inflammatory reactions in
the mammary tissue [8]. Immunomodulating agents are also normally present in human milk in
physiologically relevant quantities but there is a wide range of concentrations
of different cytokines at each time during the first 12 weeks of lactation: IL-1: 15-400 pg/mL; IL-6: 15-1032 pg/mL; TNF-alpha:
15-2933 pg/mL; Prostaglandin E2: 10-9966 pg/mL; TGF-beta1: 43-7108 pg/mL;
TGF-beta2: 208-57935 pg/mL [9].


## 1.2. Diseases of the Breast During Lactation and Stress

It is generally believed
that inflammatory breastfeeding-associated mammary diseases may be triggered or
aggravated by psychosocial stress, as observed for example in veterinary medicine. Here, exposure to experimental stressors
such as regrouping and relocation resulted into mastitis in animals, as
described for lactating ewes [10]. In humans, clinical observations
reveal similar correlations: mothers with breastfeeding-associated diseases
(milk stasis and mastitis) report an increased stress perception, that is due
to events in their social network in the weeks prior to the clinical symptoms [11].
Recent studies performed by the authors further support the alleged causality
of stress perception and puerperal diseases in humans [12].What
are the possible pathophysiological mechanisms of stress-dependent breast
diseases during lactation? The increased secretion of catecholamines in
stressed mothers impairs the release and access of oxytocin to the mammary
gland and the action of oxytocin on the secretory epithelium [13]. The release of oxytocin in response to stressful stimuli may reduce
the availibility of this hormone at the
suckling reflex. Stress  also leads to higher levels of prolactine and thus to
an increased synthesis of breast
milk. The reduced release or impaired action of oxytocin and the
coexistent higher proposal of breast milk cause an incomplete emptying of the alveoli and
galactophorus ducts and lead
to milk stasis.Stressfull
events may also cause immune supression in the mammary tissue. T-lymphocytes have
regulatory functions or act directly on foreign antigens because of producing
cytokines. T-lymphocytes are strongly involved in the defense against bacterial
invasion during mastitis [14]. These cells are
uniquely sensitive to soluble modulating factors, so it is likely that the
neuroendocrine response in stress elaborates hormones and peptides that may
have a major impact on cell mediated immunity [15]. The
increase in maternal stress perception has recently been shown to cause a
priming of the maternal immune system towards a proinflammatory, Th1-cytokine
response (IL-1, IL-6, TNF-a, INF-y) instead of anti-inflammatory Th2-cytokines
(IL-4, IL-5, IL-9 and IL-13) in the mammary tissue [12].At birth the immune
system of the neonate is primed towards a Th2 dominance. Within the first 2
years of life, the immune system is activated, probably via childhood
infections, leading to a naturally occurring shift from Th2 to Th1 immunity.
Intestinal mucosa is also premature in the first two years. Thus higher
concentrations of proinflammatory Th-1-cytokines in the breast
milk may
lead to local and systemic immunological effects of the newborn [16].


## 1.3. Modified Cytokine
Patterns of the Breast Milk and Their Effects on the
Child

Maternal stress
perception is likely intimately linked to stress reactions of the newborn.
Published data indicate that the offspring may develop somatic diseases [17], well described
for atopic dermatitis, bronchitis, and allergic
diseases in response to maternal stress perception [16, 18]. Most of
these studies focus on imprinting such as maternal stress perception
programming the child in utero,
which is generally referred to as the fetal programming hypothesis.
Surprisingly, to date, the period of lactation has received very little
attention in this context. Here, it has been described that a long period of
lactation minimizes the risk for infection of the offspring due to high levels
of IgA in breast milk, which may protect the offspring from infectious diseases [19].
However, it still remains to be elucidated if and how maternal stress
perception affects immune markers in the breast milk and whether such
alterations may have consequences for the child’s well being. Given the yet
unexplained dramatic increase of chronic inflammatory diseases in children over
the past 5 decades [20], the identification of a vicious cycle between
stress perception, impaired breastfeeding/nutrition of the offspring and the
onset of chronic diseases is urgently required and it is the aim of the present
review to foster future research in this direction.If a major part of breast diseases, as proven in our own surveys, is caused by stress and at
the same time the prevalence of these diseases is relatively high [12],
a change in the constituents of breast milk would be imaginable. One possibility
is a change in the cytokine profile in breast milk, which then might lead to
diseases in the child (Figure 1). Further, recent studies predominately arising
from rodents have elegantly shown that the epigenome of the developing fetus is
sensitive to maternal nutrition, exposure to environmental toxins as well as to
psychological stress [21]. It is postulated that exposure of the young
pup to social behavior, such as maternal care, could affect the epigenome.
Epigenetic alterations, which could have similar consequences as genetic
polymorphisms, have been shown to arise from variations of maternal behavior
and may account for differences in human behavior and possibly vulnerability to
diseases later in life of the offspring. Hence,
impaired breastfeeding could affect the growing offspring in a number of ways, that
is via an altered immune cocktail in the breast milk. But also impaired
maternal caring behavior due to discontinuation of breastfeeding may lead to
effects on the psychological development and thus on the immune system of the
newborn, because breastfeeding seems to be also very important for emotional
bonding [22].Figure 1
Vicious cycle
of increased maternal stress perception,
inflammatory breast diseases, and diseases of the newborn transmitted by
changes in the cytokine pattern in breast milk.The aim of this systematic review was to show detectable changes of
cytokines in breast milk during inflammatory processes of mammary tissue like
mastitis and possible pathological effects of these mediators on the newborn
caused by breastfeeding.


## 2. Methodology of the Present Review

In order to identify
published evidence addressing the topics (1) cytokines detectable in
inflammatory processes like a mastitis in breast milk and (2) pathological
effects of cytokines in the breast milk on the newborn, literature databases
(Medline, Embase) were searched. The following search strategies were developed
to identify the publications most sensitively.Search strategy 1: (“mastitis” [MeSH Terms] OR
mastitis [Text Word]) AND (“human milk” [Text Word] OR “milk,
human” [MeSH Terms] OR “milk” [MeSH Terms] OR milk [Text Word]) AND
(“cytokines” [MeSH Terms] OR cytokines [Text Word]); search
strategy 2: (“cytokines” [MeSH
Terms] OR cytokines [Text Word]) AND (“lactation” [MeSH Terms]) OR
(“breast feeding” [TIAB] NOT Medline [SB]) OR “breast
feeding” [MeSH Terms] OR LACTATION [Text Word]) AND (“newborn
infant” [Text Word] OR “infant, newborn” [MeSH Terms] OR
newborn [Text Word]). All articles published in German or English between 2002
until 2007 were included. This period
was established to get the most current results of this field of research.
Veterinary and human studies, experimental and clinical surveys were analysed. An overview on the process of research and
selection is shown in Figure 2.Figure 2
Flow-chart
describing the process of selection and identification of literature.


## 3. Results

Searching according to
the above-described key word strategy yielded a total of 191 publications
(titles or abstracts): after selection of the literature, 16 publications
remained (see Figure2), 10 of which referred to the first topic, 6 focussing
on the second topic. 175 of the
publications addressed none of the two topics of interest and were excluded: most
of these experimental or observation-studies described changes of cytokines in
blood (and not in breast milk) during mastitis, which was not
the focus of this review.Results from the first
search strategy are presented in Table1. All identified studies [23–32] describe
an increase of predominately proinflammatory cytokines in milk or peripheral
leukocytes in response to experimental challenge set by artificial infection
with different germs. Stress perception has not been included in the design of
these studies.Table 1
Key findings on immune alteration in breast milk, identified
upon search for the topic “cytokines detectable in inflammatory processes like
a mastitis in breast milk.”
PublicationAnimal studyHuman studyKey findingDernfalk et al. [23]+The quantification of enhanced proinflammatory cytokines IL-1beta, IL-6, and TNF-α in bovine whey or milk samples is indicative for an acute inflammatory
response of mammary tissue.Bannerman et al. [24]+Persistingly increased levels of TGF-α, -ß1, and -ß2 in milk were evident upon infection with S. aureus.Lee et al. [25]+Inflammatory cytokines (interleukin (IL)-6, IL-8, IL-12, granulocyte
macrophage-colony stimulating factor (GM-CSF), tumor necrosis factor TNF-α, and interferon (IFN)-γ, secreted by somatic cells present in the breast milk) were characterized by
real-time polymerase chain reaction (PCR) in dairy cows upon experimental
challenged with either E. coli or S. aureus.Bannerman et al. [26]+Systemic and localized bovine innate immune responses to intramammary infection withP.
aeruginosa were characterized and increased levels of IL-8, TNF-α, IL-10, and IL-12 were detected. Elevation of these cytokines was not sustained for longer than a 24-hour period.Chockalingam et al. [27]+Analysis of whey samples derived fromE. coli-infected quarters
revealed an increase of TGF-α, -ß1, and -ß2.Rambeaud et al. [28]+S. uberis challenge induced local
production of TNF-α, IL-1ß, and IL-8 in mammary tissue.Alluwaimi et al. [29]+Transcriptional activity of bovine cytokines IL-12 and TNF-α levels was significantly elevated upon experimental S. aureus infection. Levels of IL-2 were decreased. IL-12 and TNF-α levels were significantly elevated at 24 hours post-infectionem (pi)
followed by sharp decrease at 32 hours pi.Persson Waller et al. [30]+Intramammary infusion of
endotoxin fromE. coli in cows resulted in neutrophil increase in
afferent and efferent supramammary lymph nodes. Concentrations of IL-8
increased in lymph nodes. TNF-α levels increase in lymph nodes and milk. The
levels of IL-1ß increased in milk, but were not detected in lymph nodes.
Interferon-γ was undetectable.Riollet et al. [31]+IL-1α, IL-1ß, IL-6 and TNF-α, IL-10, and IL-12 mRNA were synthesized in cells derived from
infected mammary glands, whereas neither IL-2 nor IL-4 mRNA could be
detected.Prgomet et al. [32]+Cell culture models were established, where milk somatic cells and
peripheral leukocytes were cultured and activated with lipopolysaccharide
(LPS). Via real time RT-PCR, increased cytokine mRNA levels could be detected
for TNF-α, IL-6, and IL-1ß, which persisted
longer in peripheral leukocytes compared to milk somatic cells.Results from the second search strategy are
presented in Table2. Here, we identified 5 cohort studies [33–37] where
cytokine levels in breast milk were linked to different alterations or diseases
in the offspring. During revision and selection of the literature, we also identified
one further publication [38], which especially examined the influence of
cytokine-patterns on the incidence of allergies in the child. In this
publication, a correlation between these variables could not be established.
Thus, a change of cytokines in breast milk may
not have an influence on the incidence or progression of allergies.Table 2
Key findings on immune alteration in breast milk, identified
upon search for the topic “pathological effects of cytokines in the breast milk on the newborn.”
PublicationAnimal studyHuman studyKey findingZanardo et al. [33]+Levels of IL-1ß are significantly increased in colostrum from
breast-feeding mothers whose infants have hyperbilirubineamia.Moore et al. [34]+Levels of IL-7 in breast-milk, sensitive to seasonal influences, may
mediate thymus function of the newborn.Prokešová et al. [35]+Allergic mothers exhibit markedly higher IL-10 levels in breast milk
compared to healthy mothers.Rigotti et al. [36]+Lower levels of TGF-ß1 are present in mature milk of allergic mothers.Bryan et al. [37]+Breast milk from mothers of infants hospitalized with bronchiolitis had significantly higher levels of IL-2 and IL-10 compared with milk from mothers of postpartum age-matched healthy controls.Böttcher et al. [38]+There was no association between levels of IL-4, -5, -6, -8, -10, -13, -16, IFN-γ, TGF-ß1, -ß2, in the breast milk of mothers whose infants developed allergic symptoms or salivary IgA levels during the first 2 years of life. Thus, differences in the composition of cytokines and chemokines in breast milk did not, to any major degree, affect the development of atopic symptoms nor salivary IgA antibody production during the first 2 years of life.


## 4. Concluding Remarks

An increase of cytokines in breast milk has been reported from different
stages of maternal lactation: on the one hand, maternal diseases during
pregnancy—like
pre-eclampsia or allergies—can lead to a
rise in cytokines of breast milk [39]. In addition, the systematic review of the literature performed here
showed a modulation of cytokine levels in breast milk during inflammatory chest
diseases during lactation. As there are mostly only animal studies available,
it has to be investigated in humans if and to which extent levels of cytokines
are modulated in breast milk. In addition, this review revealed that an
imbalance of cytokines in breast milk may have severe consequences for the child,
which in turn affects the child's development. However, the studies summarized
here with regard to the two topics focussed on different cytokines and in
different species. Future work is needed to clear if and how these observations
can be translated into clinical significance. Further, none of these studies
included stress perception as a possible trigger for cytokine imbalances in the
breast milk. Nonetheless, it still
remains to be elucidated how stress perception may trigger inflammatory events
of the breast. Further, one may easily envision that mastitis and the related
impaired breastfeeding ability itself are potent stressors, which may
additionally aggravate the clinical symptoms. Thus, research endeavours should
focus on the identification of markers, preferably immune markers, prior to the
onset of clinical symptoms. To date, the
relationship between stress and mastitis is supported by own observations [12] and will have to be confirmed in larger collectives. However, it is nowadays
well accepted that high stress perception can alter immune hemostasis and
render the individual, both adults and newborn, less resistant to infectious diseases.
It has been suggested that this is due to increased levels of corticosteroids which can effect the functions,
pattern, and numbers of leucocytes and thus increase the host´s susceptibility
to infections [40].What are possible pathophysiological mechanisms for the shown increase
of interleukines in breast milk during inflammatory processes? The proportion
of T cells in mammary tissue normally declines during lactation and the number
of T cell subsets (CD4, CD8, and WC1-T cells in ruminants) varies significantly
during this period. The proportions of several cell populations (CD2, CD4, CD8,
MCHC II) are lower in milk than in blood following parturition, while the
proportion of WC1+ cells is higher in milk [40]. But an increase of
plasma cortisol (i.e., caused by stress) has been shown to decrease the number
of circulating lymphocytes. The number of T cells in blood declines after the
rise of serumcortisol, but expression of adhesion molecules on these cells is
not affected. This suggests that glucocorticoids can enhance migration of T
cells from blood into mammary tissues [41]. This might be important to avert inflammatory
reactions and to perpetuate the secretion of cytokines in the gland and the
breast milk.What kind of biological mechanism could be made responsible for that? So
on the one hand, a rise in cytokines of breast milk is useful to activate a
mechanism of maternal self-defence against infectious processes in the
glandular tissue [42]. On the
other hand, a rise in cytokines in breast milk could be useful in breastfed
infants in order to activate or stimulate their immunity [43]. It is
possible though that a permanent oversupply of cytokines (i.e., triggered by
high maternal stress perception) leads to an excessive stimulation/threat of
the child immune system and subsequently to the onset of diseases. This hypothesis is supported by results by
Elmlinger et al. [44] and Ustundag et al. [45] who showed that breast milk from
mothers who delivered preterm children contained lower levels of cytokines
compared to breast milk from mothers of term children. The proposal of
cytokines in maternal breast milk
seems to adapt to the requirement of the newborn and acts in accordance with
development status of the immune system. Probably the immune system of the
newborn is fragile for disruptive factors also like changes of
cytokine-concentrations mediated my breastfeeding.The review shows evidence of increased cytokines
in breast milk during inflammatory processes like mastitis and possible
pathological effects of these higher cytokine-concentrations on the newborn. A
correlation between these consequences on state of health and special interleukins
in breast milk could not be detected in the current literature and should be
investigated in further studies.



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*Source: 298760-2008-04-20.xml*