Mucosal cytokine production in small-intestinal bacterial overgrowth.
BACKGROUND
Mucosal production of interferon-gamma, interleukin-6, and tumour necrosis factor-alpha is increased in inflammatory bowel disease and parallels disease activity. Interferon-gamma production is also increased in coeliac disease. Conversely, local cytokine profiles have not been investigated in small-intestinal bacterial overgrowth. This study addressed this issue.


METHODS
Eighteen adult subjects were studies with culture of proximal small-intestinal luminal secretion and measurement of luminal interferon-gamma, interleukin-6, and tumour necrosis factor-alpha concentrations by enzyme-linked immunosorbent assay. Small-intestinal histology was assessed by light microscopy.


RESULTS
Interferon-gamma, interleukin-6, and tumour necrosis factor-alpha were measurable in proximal small-intestinal luminal secretions of all subjects, even in the absence of light microscopic evidence of enteropathy. Small-intestinal bacterial overgrowth was present in 12 of 18 (66.7%) subjects. Luminal concentrations of neither interferon-gamma nor tumour necrosis factor-alpha differed significantly in subjects with and without small-intestinal bacterial overgrowth (P + 0.06 and P = 1.0, respectively). Conversely, luminal interleukin-6 concentrations were significantly increased in subjects with this disorder (P = 0.02). Multivariate linear regression analysis suggested that colonic-type rather than salivary-type flora mediated this increased interleukin-6 response (P = 0.02 and P = 0.64, respectively). No correlation was found between luminal interleukin-6 and tumour necrosis factor-alpha concentrations, even after the confounding influence of colonic-type bacteria was excluded (P = 0.60).


CONCLUSIONS
These findings suggest that increased mucosal production of interleukin-6 occurs in small-intestinal bacterial overgrowth, particularly when the overgrowth flora includes colonic-type bacteria. Conversely, luminal levels of neither interferon-gamma nor tumour necrosis factor-alpha are increased in the circumstance, distinguishing the local cytokine profile in this disorder from those that occur in coeliac disease and inflammatory bowel disease.
Riordan
S M
SM
Dept of Gastroenterology, Prince of Wales Hospital, Sydney, Australia.
McIver
C J
CJ
Wakefield
D
D
Duncombe
V M
VM
Bolin
T D
TD
Thomas
M C
MC
D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D015169:Colony Count, Microbial; D016207:Cytokines / Q000032:analysis / Q000378:metabolism; D016099:Endoscopy, Gastrointestinal; D004797:Enzyme-Linked Immunosorbent Assay; D006801:Humans; D007371:Interferon-gamma / Q000032:analysis / Q000378:metabolism*; D015850:Interleukin-6 / Q000032:analysis / Q000378:metabolism*; D007410:Intestinal Diseases / Q000378:metabolism / Q000503:physiopathology; D007413:Intestinal Mucosa / Q000378:metabolism* / Q000382:microbiology / Q000473:pathology; D007421:Intestine, Small / Q000378:metabolism / Q000382:microbiology* / Q000473:pathology; D016014:Linear Models; D008875:Middle Aged; D015999:Multivariate Analysis; D012044:Regression Analysis; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis / Q000378:metabolism*
D016207:Cytokines; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D007371:Interferon-gamma