Given a passage with a context and an answer, construct a question on the basis of the information present in the passage. Construct the question in such a way that (i) it is unambiguous, (ii) it is answerable from the passage, (iii) its answer is unique (iv) it answer uses text phrases from the passage. Avoid creating questions that (i) can't be answered correctly without actually understanding the passage and (ii) uses the same words or phrases given in the passage.

Q: Context: Surfactant protein (SP) D shares target cells with the proinflammatory cytokine TNF-alpha, an important autocrine stimulator of dendritic cells and macrophages in the airways.', 'We sought to study the mechanisms by which TNF-alpha and SP-D can affect cellular components of the pulmonary innate immune system.', 'Cytokine and SP-D protein and mRNA expression was assessed by means of ELISA, Western blotting, and real-time PCR, respectively, by using in vivo models of allergic airway sensitization. Macrophage and dendritic cell phenotypes were analyzed by means of FACS analysis. Maturation of bone marrow-derived dendritic cells was investigated in vitro.', 'TNF-alpha, elicited either by allergen exposure or pulmonary overexpression, induced SP-D, IL-13, and mononuclear cell influx in the lung. Recombinant IL-13 by itself was also capable of enhancing SP-D in vivo and in vitro, and the SP-D response to allergen challenge was impaired in IL-13-deficient mice. Allergen-induced increase of SP-D in the airways coincided with resolution of TNF-alpha release and cell influx. SP-D-deficient mice had constitutively high numbers of alveolar mononuclear cells expressing TNF-alpha, MHC class II, CD86, and CD11b, characteristics of proinflammatory, myeloid dendritic cells. Recombinant SP-D significantly suppressed all of these molecules in bone marrow-derived dendritic cell cultures.
Answer: TNF-alpha can contribute to enhanced SP-D production in the lung indirectly through inducing IL-13. SP-D, on the other hand, can antagonize the proinflammatory effects of TNF-alpha on macrophages and dendritic cells, at least partly, by inhibiting production of this cytokine.

A: Does surfactant protein D inhibit TNF-alpha production by macrophages and dendritic cells in mice?
****
Q: Context: Expression of CINCs was regulated differentially in lipopolysaccharide-stimulated rat macrophages. We examined whether the expression of CINCs in lipopolysaccharide-stimulated rat macrophages is similarly inhibited by anti-inflammatory drugs.', 'Rat peritoneal macrophages were stimulated by lipopolysaccharide in the presence of anti-inflammatory steroids (dexamethasone, prednisolone and hydrocortisone) or non-steroidal anti-inflammatory drugs (indomethacin and piroxicam). The production and mRNA expression of three types of CINCs were measured using enzyme-linked immunosorbent assay and northern hybridization.', 'Anti-inflammatory steroids; dexamethasone, prednisolone and hydrocortisone, dose-dependently inhibited the production of CINC-1, -2 and -3, whose inhibitory patterns were similar to each other. Furthermore mRNA expression of each CINC was inhibited by dexamethasone in a dose-dependent manner. In contrast, non-steroidal anti-inflammatory drugs, indomethacin and piroxicam were without effect. Expression of each CINC was regulated differently; the production of CINC-1 reached a maximum at 12 h and then slightly decreased after lipopolysaccharide stimulation, whereas that of CINC-2 and CINC-3 increased up to 24 h. Dexamethasone inhibited the CINCs production and mRNA expression at 9 h after lipopolysaccharide stimulation.
Answer: These results indicate no difference among CINC-1, -2 and -3 in the inhibition of production and mRNA expression of CINCs by anti-inflammatory steroids, although lipopolysaccharide differentially induces expression of each CINC expression in culture of rat macrophages.

A: Is the expression of three types of CINCs by lipopolysaccharide-stimulated rat macrophages inhibited similarly by anti-inflammatory steroids?
****
Q: Context: To assess the effect of six different enteral diets on the gut barrier.', 'Laboratory study.', 'University hospital, Germany.', '70 Specific pathogen free female Crl:CDR BR rats.', 'For 7 days, 6 groups of rats were fed orally with standard chow (n = 15); total parenteral nutrition solution (oral TPN, n = 15); elemental diet (ED, n = 10); nutrient-defined diet (NDD, n = 10); or the NDD supplemented with uracil (NDD+uracil, n = 10), or fibre (NDD+fibre, n = 10).', 'Bacterial translocation to mesenteric lymph nodes, numbers of Gram negative enterobacteria and total aerobic bacteria in the caecum, and intestinal concentrations of secretory IgA.', 'The incidence of bacterial translocation was significantly increased in the groups given oral TPN, ED, NDD, and NDD+uracil compared with the group given chow. Only NDD+fibre resulted in a similar degree of translocation to that in the chow group. All groups in which there was increased translocation had a highly significant overgrowth of aerobic bacteria in the caecum, mainly by Gram negative enteric organisms. The secretory IgA concentration was reduced in the group that had been given oral TPN, and that in the ED and NDD+uracil groups was similar to that in the chow group. NDD and NDD+fibre were associated with higher intestinal concentrations of secretory IgA than chow.
Answer: Fibre-free enteral diets do not protect the gut antimicrobial barrier whatever else is in them. The superiority of early enteral as opposed to parenteral nutrition after injury may, therefore, not be the result of a specific protective effect on the gut barrier. The supplementation of commercial enteral diets with bulk fibre should be tested in clinical trials.

A:
Is fibre an essential ingredient of enteral diets to limit bacterial translocation in rats?
****