Original paper

Hydroxyapatite-coated titanium oxide ameliorates
dextran sulphate sodium-induced colitis byattenuating both innate and acquired immune
reaction
Akemi Hayakawa1,2, Hideki Kanda1, Yuzuru Kamei2, Haruhiko Suzuki1,3Organization for Promoting Life Science and Culture, Japan
Department of Plastic and Reconstructive Surgery, Nagoya University, School of Medicine, Nagoya, Japan3
Department of Immunology, Nagoya University Graduate School of Medicine, Nagoya, Japan1
2

Gastroenterology Rev 2023; 18 (1): 76–84
DOI: https://doi.org/10.5114/pg.2022.120151
Key words: titanium oxide, DSS-induced colitis.

Address for correspondence: Haruhiko Suzuki, Department of Immunology, Nagoya University Graduate School of Medicine, Nagoya,Japan, e-mail: harusuzu@med.nagoya-u.ac.jp

Abstract
Introduction: Titanium oxide (TiO2) is a widely used oxidizer for environmental management. The power of TiO2 has been
demonstrated by its photocatalytic activity. Hydroxyapatite (HA)-coated TiO2 (HA-TiO2) was used to test the in vivo effect on
dextran sulphate sodium (DSS)-induced colitis in mice.
Material and methods: Mice were monitored for body weight and then sacrificed on the seventh day, and the colon length
was measured. Their faeces were analysed for intestinal microbiota distribution, and colon tissue was subjected to histologicalexamination and immunohistochemical analysis.
Results: Weight loss was significantly lower in HA-TiO2-fed mice than in mice without HA-TiO2. The colon length in the DSS
colitis-induced mice was shortened, but HA-TiO2 feeding lessened this effect. Histological and immunohistochemical analysesof the colon revealed that macrophages and CD4+CD8+ T cells were observed in the colitis-occurring site, indicating the involvement of innate and acquired immunity in determining the degree of DSS-induced colitis. Intestinal microbiota analysis in
faeces revealed changes in the distribution of multiple bacterial species after DSS colitis induction, and the increase/decrease of
2 Clostridium (sub)clusters moved in response to the colitis phenomenon. All the described effects of HA-TiO2 were photocatalytic activity-dependent because mice that were kept in the dark showed similar results to those treated with DSS alone
without HA-TiO2.
Conclusions: HA-coated TiO2 ameliorated DSS-induced colitis through photocatalytic activity, while HA-TiO2 diminished thechanges in intestinal microbiota and immune reactions caused by DSS.

Introduction
The digestive tract is the largest frontline immune
organ that faces invasive microorganisms. Each type of
immune cell, including 60–70% of total lymphocytes, isdistributed in the intestinal tract [1]. It has recently beenshown that the immune status determined by the local
intestinal pathogens, including intestinal microbiota andparasitic worms, determines the immune condition of thetotal body, regulates the strength and specificity of theimmune reaction, and controls the onset of autoimmune
disease [2]. Immune disorder-based colitis in humans,
including the widely recognized inflammatory bowel

diseases (IBDs) such as ulcerative colitis and Crohn’sdisease, are common situations in which immune conditions involving the whole body and the pathogens exposed to the immune system affect each other.
Dextran sulphate sodium (DSS) is frequently used toinduce experimental colitis [3, 4]. DSS directly destroys
the colon area of gut epithelial cells and disrupts thephysical barrier to intestinal bacteria, causing bacteria
to invade the subepithelial area, leading to an immune
response. Simultaneously, DSS reaches the submucosal
area and is captured by antigen-presenting cells (APCs),
which stimulate T cells.

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Hydroxyapatite-coated titanium oxide ameliorates dextran sulphate sodium-induced colitis by attenuating both innate
and acquired immune reaction

Titanium oxide (TiO2) is a photocatalytic inactivatorof various materials, including environmental pollutants
and microorganisms (viruses, bacteria, etc.) [5, 6]. Most
organic materials are disassembled by the action of reactive oxygen species (ROS) that are produced by thecatalytic action of TiO2, which converts light energy to
decomposition energy. TiO2 was only activated by UVlight at ~300 nm wavelength. Therefore, doping technology using metal ions, such as Ag, Fe, and Co, arecommonly adopted. Considering its strong bactericidal
effect, TiO2 may be useful for the management of IBDs,
including colitis, because the intestinal microbiota closely affects the onset of IBD. Although this antibacterial
action may be useful for the treatment of colitis, simple
TiO2 may be harmful to mammalian host cells, including
intestinal epithelial cells, vascular endothelial cells, andimmune cells. To improve the targeting of bacteria, TiO2
is coated with hydroxyapatite (HA), which preferentiallybinds to the bacterial cell wall and prevents direct interaction between TiO2 and host cells [7, 8]. HA is a widelyused material in dental care, which has a unique feature

0

1

2

3

Day

77

of capturing bacteria and acts as a good intervention
that regulates the action of TiO2 against its target.

Aim
In this study, we investigated the effect of HA-coated TiO2 (HA-TiO2) on DSS-induced colitis in mice.

Material and methods
Mice and experimental design
Six-week-old female C57BL/6J mice were purchasedfrom SLC Japan (Hamamatsu, Japan) and maintained
under stable conditions at 25°C. The mice were divided into 4 groups: 1) normal control; 2) 4.5% DSS in
drinking water; 3) 4.5% DSS in drinking water, and fed
with 0.5 mg/day HA-TiO2; and 4) 4.5% DSS-treated plus
0.5 mg/day HA-TiO2 fed in dark condition. The mice
were kept under fluorescent light at ~800 lx throughout the experiment, except for one group kept in an
absolutely dark room throughout the experiment. The
experimental design is illustrated in Figure 1.

4

Group

Under fluorescent light

Normal

Water

5

6

7

Under fluorescent light
4.5% DSS in drinking water
4.5%DSS

Under fluorescent light
4.5% DSS in drinking water
DSS + HA-TiO2

5 mg
5 mg
5 mg
5 mg
5 mg
5 mg
HA-TiO2 HA-TiO2 HA-TiO2 HA-TiO2 HA-TiO2 HA-TiO2

5 mg
HA-TiO2

In the dark
4.5% DSS in drinking water
DSS + HA-TiO2
Dark

5 mg
5 mg
5 mg
5 mg
5 mg
5 mg
HA-TiO2 HA-TiO2 HA-TiO2 HA-TiO2 HA-TiO2 HA-TiO2

5 mg
HA-TiO2

Sacrifice and analyze

Figure 1. Design of the experiment. Mice were divided into 4 groups. Mice in the (Normal) group were kept
under fluorescent light throughout the 7 days of the experiment and were maintained with usual drinking
water. Mice in the (4.5% DSS) group were kept under fluorescent light and were treated with 4.5% dextran
sulphate sodium (DSS) in drinking water. Mice in the (DSS + HA-TiO2) group were kept under fluorescentlight, treated with 4.5% DSS in drinking water, and were daily fed with 5 mg hydroxyapatite (HA)-coatedtitanium oxide (TiO2). Mice in the (DSS + HA-TiO2Dark) group were kept in a dark place throughout the
7 days of the experiment, treated with 4.5% DSS in drinking water, and fed daily with 5 mg HA-coated TiO2.
Mice were sacrificed at 7 days after initiation of the experiment and were subjected to the analysis

Gastroenterology Review 2023; 18 (1)78

Akemi Hayakawa, Hideki Kanda, Yuzuru Kamei, Haruhiko Suzuki

 ispersing hydroxyapatite-coatedDtitanium dioxide particles
TiO2, of which approximately 10% was coated with
HA, was obtained from NANOWAVE. Co. Ltd. (Seto, Japan) [9]. Briefly, TiO2 was suspended in a pseudo-body
fluid containing a dispersant (sodium polyacrylic acid)at an even density by stirring. Sodium phosphate andcalcium chloride solutions were added to prepare theprecipitant. The precipitated HA-coated TiO2 was thensubjected to a dispersion step. The dispersion was performed using a bead-mill crusher or a jet-mill crusher.
The dispersed TiO2 was suspended in distilled water(DW) to achieve a TiO2 concentration of 10% (w/v).

 olitis induction by DSS
C
and administration of HA-TiO2
DSS 5000 (FUJIFILM, Osaka, Japan) was dissolvedin drinking water at 4.5% (w/v). The original HA-TiO2
suspension (10%) was diluted 10 times with DW, and
0.5 ml of diluted suspension containing 5 mg HA-TiO2
was forcibly fed to the subjects using plastic feeding
tubes (FTP-20-38-50, Instech Laboratories Inc., PA, USA).

Antibodies
Rabbit anti-mouse CD4 (clone 50134) and antimouse CD8 (clone 50389) monoclonal antibodies werepurchased from Sino Biologicals Inc. (Wayne, PA, USA).
Rabbit anti-mouse F4/80 antibody (clone D2S9R) was
purchased from Cell Signaling Technology Inc. (Danvers,
MA, USA).

Histology
The colon was cut into round slices, fixed with 10%
formalin for 24 h, paraffin-embedded, sectioned, deparaffinized, rehydrated, and finally stained with haematoxylin and eosin (H&E). The samples were dehydrated
and covered with water-insoluble mounting media andcover glass.

Histological score
Histological scores were blindly scored using H&Estained colonic tissue sections according to the established scoring system [10]. Points according to theseverity of changes in crypt architecture (0–3 pt), inflammatory cell infiltration (0–3 pt), muscle thickening(0–3 pt), goblet cell depletion (0–1 pt), and crypt abscess (0–1 pt) were summed for each mouse.

Immunohistochemistry
Formalin-fixed, paraffin-embedded slides were deparaffinized with xylene and then gradually rehydrated by transferring the slides from 100% EtOH to 70%

Gastroenterology Review 2023; 18 (1)EtOH. The antigen recovery process was performedby boiling the slides in citrate buffer (pH 6.4) using
microwaves. Staining with antibodies was performed
using a PolyStain DS KIT purchased from NeoBiotech(Nanterre, France). Briefly, the first primary antibody
was diluted 200 times with phosphate-buffered saline(PBS), applied to the slides, incubated in a humidified
chamber for 40 min at room temperature, then washed
3 times with PBS-tween20 (PBS-T). The secondary antirabbit IgG antibody-alkaline phosphatase polymer wasapplied and incubated for 20 min, washed with PBS-T,
and incubated for 10 min with a mixture of permanent
red substrate, activator, and chromogen. After vigorous
washing, inactivator A was applied and incubated for
30 min, followed by 5 min of incubation with inactivator
B, then washed with PBS-T, incubated with the second
primary antibody for 40 min, washed with PBS-T, andincubated with the secondary anti-rabbit IgG antibody,horseradish peroxidase (HRP), for 20 min. After counterstaining with 5-times diluted haematoxylin solution andwashing, emerald chromogen was applied to the slides
and incubated for 5 min. The slides were then washedand dried at 85°C for 10 min. The stained specimens
were fixed with 100% methanol, dehydrated with 100%
ethanol and xylene, and mounted with water-insoluble
mounting media and cover glass.

Numbers of infiltrated cells
Immunohistochemically stained colon sections weremicroscopically examined using a 20× objective lensand viewed on a PC display. The number of cells stainedwith the expected colour was counted for 3 randomly
selected fields, and the sum of 2 independent sections
for each mouse was calculated.

I ntestinal microbiota analysis of mouse
faeces
Mouse faeces were obtained from the colon after
the mice were sacrificed. DNA was extracted from thesamples and amplified for a specific sequence, and eachfragment was sequenced. The number of fragments
identified as specific bacterial species based on their
DNA sequences was analysed. The intestinal microbiota analysis was performed by TechnoSuruga LaboratoryCo., Ltd. (Shizuoka, Japan).

Ethics Committee Approval
The authors declare that the research was conducted according to the principles of the Regulations on Animal Experiments in Nagoya University and approved(approval number 31412) by the Centre for Anima
Research and Education, Nagoya University Graduate
School of Medicine, Japan.

Hydroxyapatite-coated titanium oxide ameliorates dextran sulphate sodium-induced colitis by attenuating both innate
and acquired immune reaction

The graphic data are presented as mean values,
with error bars of standard deviation. Statistical comparisons between the 2 groups were performed using
Student’s t-test.

Results
Body weights were calculated daily (Figure 2). Apparent body weight loss was observed 6 days after the
initiation of DSS administration. Although body weightloss was also observed in HA-TiO2-fed mice, the loss
was significantly lower than that in the DSS-treatedmice (Figure 2).
To evaluate the severity of colitis, the colon length
was measured when the mice were sacrificed 7 days
after the initiation of DSS administration. As shown in
Figures 3 A and B, the colon length of DSS-treated mice
was shorter than that of untreated mice. This reduction
in colon length was significantly improved by the administration of HA-TiO2 (Figure 3 B).
Weight loss was observed in the group of mice kept
in the dark throughout the 7 days of the experiment
similarly to those treated with DSS without HA-TiO 2
feeding (Figure 2). Furthermore, the improvement incolon length by HA-TiO2 feeding was not significant inmice kept in the dark, and the colon length was significantly different between HA-TiO2-fed mice kept in
the dark and those exposed to light (Figure 3 B). Theseobservations support the photo-dependent activity of
TiO2 for the amelioration of DSS-induced colitis.
Histological examination of the colon was performed using H&E-stained tissue sections. Figure 4
shows the typical pathogenic changes in each of the
4 experimental groups. In all the sections examined,
DSS-treated mice without TiO2-administration showedstrong signs of inflammation associated with disruptionof mucosal epithelium, thickening of both mucosal andsubmucosal layers, and massive infiltration of inflammatory cells (Figure 4 B). In contrast, the pathologicalsigns in the colons of HA-TiO2-fed mice were dramatically improved, even though they were treated withdrinking water containing the same concentration of
DSS. In general, the examined sections were mostly intact (Figure 4 C). However, the colons of mice that werefed with HA-TiO2 but were kept in the dark showedpathological images of inflammatory signs similar to
those treated with DSS alone (Figure 4 D). These histological findings were confirmed by scoring (Figure 4 E).
The histological score was significantly reduced in DSS
plus HA-TiO2-treated mice exposed to light comparedwith that in DSS-treated mice, but not in DSS plus HATiO2-treated mice kept in the dark. This result indicatesthe importance of light on the effects of TiO 2. Thus,

judging from the changes in body weight, length of thecolon, and pathological examination of the colon, it was
confirmed that HA-coated TiO2 can prevent more severe
progression of DSS-induced acute colitis depending on
its photocatalytic activity.
When TiO2 was not appropriately coated with HA,
the results were inconclusive (data not shown), implying that coating TiO2 with HA is crucial for its activity.
Macrophages and CD4+ or CDF8+ T cells were detected in the colon tissue by immunohistochemical analysis
using anti-F4/80 monoclonal antibody (mAb) and anti-CD4/CD8 mAbs to detect macrophages and T cells, respectively. As shown in Figure 5, a considerable numberof macrophages were observed in the colon tissue ofmice with DSS-induced colitis (Figure 5 B), whereas theymostly disappeared in the colon tissue of mice treatedwith HA-coated TiO2 (Figure 5 C). Macrophages re-appeared in the colon tissue of mice who were treatedwith HA-coated TiO2 but remained in the dark (Figure5 D). The number of infiltrated macrophages was significantly reduced in DSS plus HA-TiO2-treated mice exposed to light, compared with that in DSS-treated mice,but not in DSS plus HA-TiO2-treated mice kept in the
110
105
100
95
%

Statistical analysis

79

90
85
80
75
		 2

3

NormalDSS + HA-TiO2

4
Day

5

6

7

8

4.5% DSS
DSS + HA-TiO2-Dark

Figure 2. Body weight of mice with DSS-induced
colitis. Mice were maintained with usual drinking water (Normal, black line, n = 2), with 4.5%
DSS-containing water (4.5% DSS, blue line, n = 6),
with 4.5% DSS-containing water fed with
5 mg/day of HA-TiO2 (DSS + HA-TiO2, red line,n = 5), or maintained in the dark with 4.5% DSS
in drinking water fed with 5 mg/day HA-TiO2(DSS + HA-TiO2-Dark, yellow line, n = 5). Mice
were kept under fluorescent light at ~800 Lux
except for the group maintained in the dark. Averages with error bars of standard deviation arepresented as percentages of initial body weight(day 0). Significantly different (*0.01 < p < 0.05,**p < 0.01). Not significantly different (†p > 0.05)

Gastroenterology Review 2023; 18 (1)80

Akemi Hayakawa, Hideki Kanda, Yuzuru Kamei, Haruhiko Suzuki

A

B
11

Normal109Colon length [cm]84.5% DSS

7

6
DSS + HA-TiO2
5

4
DSS +
HA-TiO2-Dark
3
Normal

4.5% DSS

DSS + HA-TiO2

Dark

Figure 3. Colon of mouse with DSS-induced colitis. Mice were sacrificed at 7 days after initiation of theexperiment. A – Macroscopic appearance of the colon. Note the massive haemorrhage and diarrhoea stool
in the DSS colon. Such haemorrhage and diarrhoea disappeared in mice fed with HA-TiO2. B – Colon length.
Box and whisker plot showing box as lower and upper quartile and whisker as minimum and maximum
values in each group (n = 6 for control, n = 10 for 4.5% DSS, n = 12 for DSS + HA-TiO2, and n = 10 for DSS+ HA-TiO2 kept in the dark). Significantly different (*0.01 < p < 0.05, **p < 0.01). Not significantly different(†p > 0.05)
dark (Figure 5 E). T cells were examined using the CD4
and CD8 markers. Massive inflammatory cell infiltration
was observed in the colon of DSS-treated mice, and thisinfiltrate was abundant in CD4+ and CD8+ T cells (Figure
6 B). Such T-cell infiltrates were absent from the colon
of HA-TiO2-treated mice exposed to fluorescent light(Figure 6 C), but they were observed in mice kept in thedark (Figure 6 D). Both the numbers of infiltrated CD4+
cells and CD8+ cells were significantly reduced in DSS
plus HA-TiO2-treated mice exposed to light comparedwith that in DSS-treated mice but not in DSS plus HATiO2-treated mice kept in the dark (Figure 6 E). Thus,
macrophages and T cells appeared to be involved in theprocess of DSS-induced colitis and its amelioration by
HA-TiO2.
Intestinal microbiota were analysed for faeces obtained from DSS-treated mice, either with or without
HA-coated TiO2. Figure 7 shows obvious changes in the

Gastroenterology Review 2023; 18 (1)species of bacteria residing in the mouse colon. Analysisof the intestinal microbiota revealed that the components of the bacteria dramatically changed after DSS
treatment. In brief, Lactobacillus, Prevotella, and Clostridium cluster XVIII were relatively decreased, while
Clostridium subcluster XIVa and Clostridium cluster XI
were increased. Among these changes, Lactobacillus,
Prevotella, and Clostridium XVIII, which were decreased
by DSS treatment, were all unchanged by HA-TiO2 treatment. In contrast, Clostridium subclusters XIVa and XI,
which are increased by DSS treatment, were decreased
by HA-TiO2 treatment. A decrease in Clostridium cluster
XI, which is possibly linked with the increase in Bacteroides, may be crucial for the activity of HA-TiO2.

Discussion
Our results are in contrast to previous results for
TiO2 nanoparticles that exacerbated DSS-induced coli-Hydroxyapatite-coated titanium oxide ameliorates dextran sulphate sodium-induced colitis by attenuating both innate
and acquired immune reaction

A

B

C

D

81

E

10
9
8
7
6
5
4
3
2
1
0

Normal
DSS
DSS +
DSS +
			HA-TiO2
HA-TiO2				 Darktis [11–13]. The different results may indicate a fundamental difference in the relationship between the TiO2
nanoparticles and HA-coated TiO2. As assumed before
our work, simple TiO2 nanoparticles may directly interact with mouse intestinal epithelial cells (IECs), macrophages, and dendritic cells, performing photocatalytic
activity on these cells [14]. In the case of HA-coated
TiO2, direct interaction of TiO2 with mouse cells could

Figure 4. Histological analysis of the colon. Normal (A), 4.5% DSS-treated (B), DSS-treated and
HA-TiO2 fed (C), and DSS-treated and HA-TiO2
fed-kept in the dark (D). Mice were sacrificed
at day 7, and their colon sections were stainedwith haematoxylin and eosin. Pictures with typical changes representing each group are shown.
All the pictures were taken with a 10× objective
lens. E – Histological scores were calculated andthe average of 3 mice in each group are shownwith error bars of standard deviation. Significantly different (*0.01 < p < 0.05, **p < 0.01).
Not significantly different (†p > 0.05)
be avoided with HA. To succeed in the experiment described in this study, there are 2 important points toconsider. First, TiO2 was coated with HA. The coatingprocess of TiO2 by HA is crucial because incomplete
coating processes or HA alone do not show colitis-suppressing activity (data not shown). In addition to theabove-mentioned protective activity of HA in mouse
cells, HA preferentially binds to the bacterial cell wall

Gastroenterology Review 2023; 18 (1)82

Akemi Hayakawa, Hideki Kanda, Yuzuru Kamei, Haruhiko Suzuki

A

B

C

D

E

160
140
120
100
80
60
40
20
0

Normal
DSS
DSS +
DSS +
HA-TiO2
			HA-TiO2				 Dark

and possibly maintains its position in the intestinal lumen. Secondly, light is required for the activity of TiO2.
The mice were exposed to fluorescent light. Because
we used Fe-doped HA-TiO2, TiO2 is activated not only
by UV light but also by a wide range of visible light.
Fluorescent light, including near infrared light, can infiltrate the skin, abdominal wall, and intestinal wall of
mice, activating TiO2 in the intestinal lumen [15]. We

Gastroenterology Review 2023; 18 (1)Figure 5. Immunohistochemical analysis detecting macrophage-specific molecule F4/80. Normal
control (A), 4.5% DSS-treated (B), DSS-treatedand HA-coated TiO2 fed (C), DSS-treated and
HA-TiO2 fed-kept in the dark (D). F4/80-expressing macrophages are shown by Permanent Red
staining and indicated by red arrows. Pictureswith typical changes representing each groupare shown. All the pictures were taken witha 20× objective lens. E – Numbers of macrophages were calculated, and the average of
3 mice in each group are shown with error barsof standard deviation. Significantly different(*0.01 < p < 0.05, **p < 0.01). Not significantly
different (†p > 0.05)
performed an experiment in which mice were kept in
the dark without any exposure to light for 7 days andshowed that HA-coated TiO2 did not affect DSS-induced
colitis. Although this result is important, suggesting therequirement of light for the photocatalytic activity of
TiO2, the other conditions of the mice could not be controlled to the same level, leaving the possibility that theresults are not validated.

Hydroxyapatite-coated titanium oxide ameliorates dextran sulphate sodium-induced colitis by attenuating both innate
and acquired immune reaction

A

B

C

D

E

140
120
100
80
60
40
20
0

Normal
DSS
DSS +
DSS +
			HA-TiO2
HA-TiO2				 Dark
CD4+
CD8+

DSS affects innate immunity by influencing macrophages [16, 17]. Recent studies have shown that there
are 2 different types of macrophages: one with the usual activity that positively correlates with the strength of
the immune response and one that suppresses the immune response. It has been reported that DSS may affect both types of macrophages, thus complicating theresults of the immune response in DSS-induced colitis.

83

Figure 6. Immunohistochemical analysis of
the colon for CD4 and CD8 expression. CD8
was stained with Permanent Red and CD4
was stained with Emerald. Normal colon ofa control mouse (A), 4.5% DSS-treated colon(B), DSS-treated and HA-TiO 2-fed colon (C).
DSS-treated and HA-TiO2 fed colon kept in thedark (D). Pictures with typical changes representing each group are shown. CD8+ cells arestained with Permanent Red and indicated by
red arrows. CD4+ cells are stained with Emerald
and indicated by green arrows. All the pictures
were taken with a 40× objective lens. E – Numbers of CD4+ cells and CD8+ cells were calculated, and the average of 3 mice in each group areshown with error bars of standard deviation. Significantly different (*0.01 < p < 0.05, **p < 0.01).
Not significantly different (†p > 0.05)
DSS also affects acquired immunity [18–20]. In thecase of DSS-induced colitis, the cells that infiltrated
the swollen submucosal area contained CD4+ and CD8+
T cells, indicating that the acquired immune system wasworking 7 days after the initiation of the DSS-induced
colitis treatment. HA-TiO2 also decreased the numberof infiltrated T cells, although it is more likely that HATiO2 caused changes in the intestinal microbiota that

Gastroenterology Review 2023; 18 (1)84

Akemi Hayakawa, Hideki Kanda, Yuzuru Kamei, Haruhiko Suzuki

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Bacteroides
Clostridium cluster IV
Clostridium cluster XI
Lactobacillales
Prevotella
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Figure 7. Intestinal microbiota analysis. Averages
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16.
Zhang R, Ito S, Nishio N, et al. Dextran sulphate sodium incolitis in mice. The changes in intestinal microbiota andcreases splenic Gr1+CD11b+ cells which accelerate recovery
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Conflict of interest
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The authors declare no conflict of interest.
2011; 10: 39-46.
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photocatalytic antibacterial activity of Ni-doped and N-doped
TiO2 on Staphylococcus aureus and Escherichia coli bacteria.
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NormalGastroenterology Review 2023; 18 (1)