GEO-PGS also had ameliorating effect on enteritis and intestinal dysfunction in vivo, which might be related to the inhibition of gene expression of inflammatory cytokines (TLR2, IL-6, TNF<sub>α</sub>, and IL-8).
The results showed that, compared with the control group, dietary CT (1) induced intestinal histopathological lesions and aggravated enteritis; (2) decreased the lysozyme and acid phosphatase activities, complement 3 (C3), C4 and immunoglobulin M contents, and down-regulated the Hepcidin, liver-expressed antimicrobial peptide(LEAP)-2A, LEAP-2B, Mucin2 and β-defensin-1 mRNA levels in the proximal intestine (PI), mid intestine (MI) and distal intestine (DI) (P < 0·05); (3) down-regulated the mRNA levels of anti-inflammatory cytokines transforming growth factor (TGF)-β1, TGF-β2 (not in MI and DI), IL-4/13A (not IL-4/13B), IL-10 and IL-11 partly correlated with target of rapamycin (TOR) signalling; (4) up-regulated the mRNA levels of pro-inflammatory cytokines interferon-γ2 (IFN-γ2), interleukin-1β (IL-1β), IL-6, IL-8 (not in PI), IL-12p35, IL-12p40, IL-15 and IL-17D partly related to nuclear factor kappa B (NF-κB) signalling in the intestine of on-growing grass carp.
The results showed that, compared with the control group, dietary CT (1) induced intestinal histopathological lesions and aggravated enteritis; (2) decreased the lysozyme and acid phosphatase activities, complement 3 (C3), C4 and immunoglobulin M contents, and down-regulated the Hepcidin, liver-expressed antimicrobial peptide(LEAP)-2A, LEAP-2B, Mucin2 and β-defensin-1 mRNA levels in the proximal intestine (PI), mid intestine (MI) and distal intestine (DI) (P < 0·05); (3) down-regulated the mRNA levels of anti-inflammatory cytokines transforming growth factor (TGF)-β1, TGF-β2 (not in MI and DI), IL-4/13A (not IL-4/13B), IL-10 and IL-11 partly correlated with target of rapamycin (TOR) signalling; (4) up-regulated the mRNA levels of pro-inflammatory cytokines interferon-γ2 (IFN-γ2), interleukin-1β (IL-1β), IL-6, IL-8 (not in PI), IL-12p35, IL-12p40, IL-15 and IL-17D partly related to nuclear factor kappa B (NF-κB) signalling in the intestine of on-growing grass carp.
ZBEO also had an inhibitory effect on enteritis and intestinal dysfunction induced by infection of E. coli in vivo, and histopathological observation indicated that ZBEO could markedly ameliorate the structural destruction of intestinal tissues, which might be related to its inhibitory effect on the gene expression of inflammatory cytokines (TLR2, TLR4, TNF<sub>α</sub> and IL-8).
Our previous studies demonstrated that phase variation to specific "successful alleles" at C. jejuni contingency loci Cj0045 (successful alleles carry 9G or 10G homopolymeric tracts) and Cj0170 (successful allele carries a 10G homopolymeric tract) in C. jejuni populations is strongly associated with colonization and enteritis in C57BL/6 IL-10 deficient mice.
Furthermore, when the IL-10 gene is inactivated as in C3Bir tlr4(-/-) IL-10(-/-) mice, enteritis and intensive extraintestinal spread were observed, suggesting that clinical presentations of C. jejuni infection are controlled by a complex interplay of factors.
Our results suggest that the Ras/MAPK cascade acts as the upstream signaling for AP-1 activation and IL-8 expression in toxin A-stimulated intestinal epithelial cells and may be involved in the development of enteritis after infection with toxin A-producing C. difficile.
The results showed that, compared with the control group, dietary CT (1) induced intestinal histopathological lesions and aggravated enteritis; (2) decreased the lysozyme and acid phosphatase activities, complement 3 (C3), C4 and immunoglobulin M contents, and down-regulated the Hepcidin, liver-expressed antimicrobial peptide(LEAP)-2A, LEAP-2B, Mucin2 and β-defensin-1 mRNA levels in the proximal intestine (PI), mid intestine (MI) and distal intestine (DI) (P < 0·05); (3) down-regulated the mRNA levels of anti-inflammatory cytokines transforming growth factor (TGF)-β1, TGF-β2 (not in MI and DI), IL-4/13A (not IL-4/13B), IL-10 and IL-11 partly correlated with target of rapamycin (TOR) signalling; (4) up-regulated the mRNA levels of pro-inflammatory cytokines interferon-γ2 (IFN-γ2), interleukin-1β (IL-1β), IL-6, IL-8 (not in PI), IL-12p35, IL-12p40, IL-15 and IL-17D partly related to nuclear factor kappa B (NF-κB) signalling in the intestine of on-growing grass carp.
GEO-PGS also had ameliorating effect on enteritis and intestinal dysfunction in vivo, which might be related to the inhibition of gene expression of inflammatory cytokines (TLR2, IL-6, TNF<sub>α</sub>, and IL-8).
Moreover, IL-6 was highly expressed in peripheral blood and colonic mucosa samples genotyped as CC compared to those in TT and TC groups, furthermore, IL-6 was highly expressed in peripheral blood and colonic mucosa samples from participants with enteritis than without enteritis, whereas let-7 was highly expressed in peripheral blood and colonic mucosa samples genotyped as TT and TC compared to those in CC groups.
GEO-PGS also had ameliorating effect on enteritis and intestinal dysfunction in vivo, which might be related to the inhibition of gene expression of inflammatory cytokines (TLR2, IL-6, TNF<sub>α</sub>, and IL-8).
Lymphocytic enteritis associated to celiac disease shows an increase of FOXP3 expression and lymphocytes T-γδ that is not detected in other etiologies of enteritis.
ZBEO also had an inhibitory effect on enteritis and intestinal dysfunction induced by infection of E. coli in vivo, and histopathological observation indicated that ZBEO could markedly ameliorate the structural destruction of intestinal tissues, which might be related to its inhibitory effect on the gene expression of inflammatory cytokines (TLR2, TLR4, TNF<sub>α</sub> and IL-8).
ZBEO also had an inhibitory effect on enteritis and intestinal dysfunction induced by infection of E. coli in vivo, and histopathological observation indicated that ZBEO could markedly ameliorate the structural destruction of intestinal tissues, which might be related to its inhibitory effect on the gene expression of inflammatory cytokines (TLR2, TLR4, TNF<sub>α</sub> and IL-8).
C3H/HeJ tlr4(-/-) mice that specifically express the Cdcs1 allele showed colonization and limited extraintestinal spread without enteritis implicating this interval in the clinical presentation of C. jejuni infection.
The cst-II gene is responsible for the development of Guillain-Barré and Fisher syndromes, and the polymorphism (Thr/Asn51) determines which syndrome develops after C. jejuni enteritis.
The cst-II gene is responsible for the development of Guillain-Barré and Fisher syndromes, and the polymorphism (Thr/Asn51) determines which syndrome develops after C. jejuni enteritis.
However, the identification of apparently nonexpressed, atypical cpb2 genes raises the question of whether this protein plays the same role in enteritis in other animal species.
The correlation between enteritis in other animal species and the presence of cpb2 was not so strong. cpb2 was found in 21.4% of C. perfringens isolates from cattle with enteritis, and in 47.3% of isolates from calves with enteritis or abomastitis.