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. 2015 Jun;31(6):615-22.
doi: 10.1089/AID.2014.0085. Epub 2015 Apr 8.

"VSports app下载" Chronic HIV Infection Is Associated with Upregulation of Proinflammatory Cytokine and Chemokine and Alpha Defensin Gene Expression in Colorectal Mucosa

Jennifer Mait-Kaufman  1 , Esra Fakioglu  1 , Pedro M M Mesquita  1   2 , Julie Elliott  3 , Yungtai Lo  4 , Rebecca Pellett Madan  1
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Chronic HIV Infection Is Associated with Upregulation of Proinflammatory Cytokine and Chemokine and Alpha Defensin Gene Expression in Colorectal Mucosa

Jennifer Mait-Kaufman (VSports注册入口) et al. AIDS Res Hum Retroviruses. 2015 Jun.

Abstract

HIV may induce gastrointestinal (GI) mucosal immune dysregulation similar to inflammation observed in ulcerative colitis (UC) VSports手机版. Colorectal biopsies from healthy controls (N=12) and from participants with HIV (N=20) or UC (N=9) were subjected to real time (RT)-PCR for selected cytokines, chemokines, antimicrobial peptides, Toll-like receptors, and inflammatory signaling and epithelial barrier proteins. HIV long terminal repeat relative copy number (RCN) in HIV participant biopsies was quantified by RT-PCR. Mean interleukin (IL)-6 mRNA levels did not differ significantly between HIV and UC participants (p=0. 48) but were significantly higher relative to control mRNA levels only for HIV participants (p=0. 03). Mean IL-8 and human defensin (HD) 5 mRNA levels were similar between HIV and UC participants (p=1. 0 and p=0. 35, respectively) and were significantly greater in both groups relative to controls (p<0. 05 for all). Human beta-defensin (HBD)-2 mRNA levels were higher in UC relative to HIV and control participants (p<0. 01 for both). Conversely, HBD-1 mRNA levels were downregulated in UC vs. HIV participants (p=0. 01). Mediator gene expression did not differ significantly between HIV participants with detectable (N=10) or nondetectable (N=10) plasma viral loads. Tissue HIV relative copy number (RCN) correlated with plasma viral load (r=0. 88, p<0. 01) but not with mediator mRNA levels. The results of this study indicate that both chronic HIV infection and UC are associated with similar patterns of IL-6, IL- 8, and HD5 expression in colorectal biopsy tissue. These findings suggest overlapping mechanisms for GI mucosal inflammation in these two illnesses and merit further investigation in larger studies. .

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Figures

<b>FIG. 1.</b>
FIG. 1.
Histological grading scale (grades 1–6) illustrated using representative hematoxylin–eosin-stained sections of colonic mucosa. Grade 1: Intact epithelium and lamina propria. No structural abnormality. Grade 2: Detatched epithelium but intact lamina propria. Chronic inflammatory cell infiltrates. Grade 3: Detached epithelium and disaggregated lamina propria. Neutrophil infiltrates in lamina propria. Grade 4: Detached epithelium and disaggregated lamina propria with >30% karyorrhexis. Neutrophil infiltrates in epithelium. Grade 5: Detached epithelium and disaggregated lamina propria with >75% karyorrhexis and crypt destruction. Grade 6: Epithelium lost and minimal cellular remnants, with mostly structural elements remaining and erosions or ulcerations present. Biopsy samples scored as grade 1 were categorized as normal. Samples scored as grades 2–3 were categorized as having mild changes, grade 4 samples were categorized as moderate, and grades 5–6 were categorized as severe.
<b>FIG. 2.</b>
FIG. 2.
mRNA for interleukin (IL)-6, IL-8, human defensin (HD)5, human β defensin (HBD)-1, HBD-2, and MyD88 was quantified from biopsy tissue by real time (RT)-PCR. mRNA levels were log-transformed, expressed relative to large ribosomal protein (RPLPO), and compared across groups by one-way analysis of variance (ANOVA) followed by Bonferroni correction for post hoc pairwise comparisons. As a secondary analysis, HIV-infected participants (all HIV) were stratified by detectable (HIVDVL) vs. nondetectable (HIVNDVL) plasma viral load; mRNA levels did not differ significantly for any mediator between the HIVDVL and HIVNDVL groups (p>0.05 for all). (a) Mean IL-6 mRNA levels did not differ significantly between ulcerative colitis (UC) and all HIV participants (p=0.48) but were significantly higher in all HIV participants vs. controls. (b) IL-8 mRNA levels were similar between UC and all HIV participants (p=1.0) and differed significantly in both groups from those observed in controls. (c) Mean HD5 mRNA levels were similar between UC and all HIV participants (p=1.0) but were significantly higher in both groups relative to controls. (d) Mean HBD-1 mRNA levels were significantly lower in UC compared to all HIV participants. (e) Mean HBD-2 levels were significantly higher in UC compared to all HIV and control participants. (f) Mean MyD88 mRNA levels were significantly higher in UC compared to all HIV participants.
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References

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