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.
Dept of Gastroenterology, Prince of Wales Hospital, Sydney, Australia.
S M
SM
Riordan
C J
CJ
McIver
D
D
Wakefield
V M
VM
Duncombe
T D
TD
Bolin
M C
MC
Thomas
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