Info

Human

Lb. acidophilus + Lactobacil-lus GG

Decreased shigellosis-associated diarrhea

(66)

Abbreviations: Bif, Bifidobacterium; C, Clostridium; E, Escherichia; L, Listeria; Lb, Lactobacillus; Sc, Saccharomyces; Str, Streptococcus.

Abbreviations: Bif, Bifidobacterium; C, Clostridium; E, Escherichia; L, Listeria; Lb, Lactobacillus; Sc, Saccharomyces; Str, Streptococcus.

to trigger the antibody response rapidly so that it interfered with further viral activity. Animal studies do indicate that secretory IgA can be triggered by probiotic ingestion (72), but the rate was not determined, nor was the influence on cessation of fluid loss across the secretory cell membranes. Modification of the cytokine profile to one that enhances anti-inflammatory cytokines (73) or attenuation of the virus' and/or toxin's effect on the enteric nervous system might provide rapid cessation of epithelial secretion and diarrhea. Alternatively, stimulation of T cells to produce gamma interferon, leading to potential inhibition of chloride secretion, might also inhibit diarrhea. One aspect of the immunity theory that needs to be clarified is why lactobacilli, which we assume are present in the child intestine, appear unable to prevent infection; yet those administered orally thereafter help to clear the diarrhea.

A third mechanism could involve a signal(s) from probiotics to the host that down-regulates the secretory and motility defenses designed to remove perceived noxious substances. Glycosylated intestinal mucins inhibit rotaviruses (74), and MUC2 and MUC3 mRNA expression is increased in response to probiotics signaling, protecting cells against pathogenic bacterial adhesion (13). However, direct host cell signaling between probiotic organism and secretory cells has not yet been investigated. Attachment of the virus causes cytokine prostaglandin and nitric oxide to be released from the enterocytes, both of which could affect motility. The possibility exists that lactobacilli could alter this release (75). The intestinal host defense mechanisms comprise complex systems involving the innate and adaptive immune responses, and protective effects of the indigenous microbiota. The commensal microorganisms colonizing the intestinal mucosa provide a barrier effect against pathogens by using a variety of mechanisms, such as occupation of habitats, competition for nutrients, and production of antimicrobials. It is also established that the probiotic organisms can modulate the homeostasis of the host's defense mechanisms, both innate and adaptive immune functions (4).

A final theory is that the probiotics produce substances that inactivate the viral particles. This has been shown in vitro (76), with supernatants from Lactobacillus rhamnosus GR-l and L. fermentum RC-14 inactivating 109 particles of the double-stranded DNA adenovirus and the negative-stranded RNA vesicular stomatitis virus within 10 minutes. The effect was likely due to acid, but more specific antiviral properties have not been ruled out. Whether or not viral inactivation can inhibit diarrhea remains to be confirmed.

Figure 1 Schematic representation of the possible ways by which probiotics may counteract (0) the intestinal inflammatory process. Source: From Ref. 68.

Figure 1 Schematic representation of the possible ways by which probiotics may counteract (0) the intestinal inflammatory process. Source: From Ref. 68.

More detailed investigation is needed to understand how probiotic strains reduce the duration of diarrhea in conjunction with rehydration therapy. Such studies could lead to a better understanding of the dynamics within the intestinal microbiota that is being disrupted and depleted by rapid fecal loss. In doing so, new intervention therapies should be generated to quickly and effectively trigger the cessation of not only rotavirus infections but also other gastrointestinal infections that debilitate patients for 2 to 3 days.

The possible mode of action for diarrhea and other gastrointestinal diseases, such as IBS and IBD, are the subject of intense investigation in many labs, using genomics, knockout mice models, etc., (77,78).

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