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Modified Sweat Glands and LPS

Mammary glands are enlarged and modified sweat glands.[1] It is well known in the dairy industry that cows infected by certain bacteria produce less milk. The first article on this page shows that cows infected by Escherichia coli produce less milk. Escherichia coli is a gram negative bacteria that contains LPS (lipopolysaccharide) in its cell wall. The second article shows that lipopolysaccharide is responsible for the harmful cytokin response.

Click here to view this article on PubMed

1: Vet Res. 2008 Mar-Apr;39(2):18. Epub 2008 Jan 29.

Escherichia coli, but not Staphylococcus aureus triggers an early increased expression of factors contributing to the innate immune defense in the udder of the cow.

Petzl W, Zerbe H, Günther J, Yang W, Seyfert HM, Nürnberg G, Schuberth HJ.

Clinic for Ruminants, Ludwig-Maximilians-University, Munich, Germany.

The outcome of an udder infection is influenced by the pathogen species. We established a strictly defined infection model to better analyze the unknown molecular causes for these pathogen-specific effects, using Escherichia coli and Staphylococcus aureus strains previously asseverated from field cases of mastitis. Inoculation of quarters with 500 CFU of E. coli (n = 4) was performed 6 h, 12 h, and 24 h before culling. All animals showed signs of acute clinical mastitis 12 h after challenge: increased somatic cell count (SCC), decreased milk yield, leukopenia, fever, and udder swelling. Animals inoculated with 10 000 CFU of S. aureus for 24 h (n = 4) showed no or only modest clinical signs of mastitis. However, S. aureus caused clinical signs in animals, inoculated for 72 h-84 h. Real-time PCR proved that E. coli inoculation strongly and significantly upregulated the expression of beta-defensins, TLR2 and TLR4 in the pathogen inoculated udder quarters as well as in mammary lymph nodes. TLR3 and TLR6 were not significantly regulated by the infections. Immuno-histochemistry identified mammary epithelial cells as sites for the upregulated TLR2 and beta-defensin expression. S. aureus, in contrast, did not significantly regulate the expression of any of these genes during the first 24 h after pathogen inoculation. Only 84 h after inoculation, the expression of beta-defensins, but not of TLRs was significantly (> 20 fold) upregulated in five out of six pathogen inoculated quarters. Using the established mastitis model, the data clearly demonstrate a pathogen-dependent difference in the time kinetics of induced pathogen receptors and defense molecules.

PMID: 18258172 [PubMed - indexed for MEDLINE


Click here to view this article on PubMed

1: Am J Vet Res. 2005 Sep;66(9):1590-7

. Cytokine response of bovine mammary gland epithelial cells to Escherichia coli, coliform culture filtrate, or lipopolysaccharide.

McClenahan DJ, Sotos JP, Czuprynski CJ.

Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin, Madison, WI 53706, USA.

OBJECTIVE: To define the cytokine response of a cultured mammary gland epithelial cell line (ie, Mac-T) when incubated with Escherichia coli or its products. SAMPLE POPULATION: Mac-T cells and E coli from cows with mastitis. PROCEDURE: Mac-T cells were incubated with E coli or its products. The cytokine response of Mac-T cells to these treatments was quantified by measuring mRNA content of interleukin (IL)-1alpha, IL-1beta, IL-8, and tumor necrosis factor (TNF)-alpha by use of a quantitative reverse transcriptase-polymerase chain reaction assay. The amount of TNF-alpha secreted was also measured. RESULTS: Treatment with E coli or its products resulted in significant increases in IL-1alpha, IL-8, and TNF-alpha mRNA content in Mac-T cells. This increase was reversible when culture filtrate was incubated with polymyxin B. The amount of IL-1beta mRNA in Mac-T cells increased only slightly over baseline after treatment with E coli or its products, but this increase was not diminished by incubation of E coli filtrate with polymyxin B. CONCLUSIONS AND CLINICAL RELEVANCE: Incubation of Mac-T cells with E coli or its products resulted in increased amounts of IL1alpha, IL-8, and TNF-alpha mRNA. Inhibition of this response by incubation of culture filtrate with polymyxin B suggested that lipopolysaccharide was the main bacterial product that stimulated the cytokine response. The small increase in IL-1beta content in Mac-T cells incubated with E coli or its products suggested that this cytokine had a smaller role in the Mac-T cell response to E coli.

PMID: 16261834 [PubMed - indexed for MEDLINE]

References

[1] Human Anatomy and Physiology, by Van Wynsberghe, Noback and Carok, published by McGraw-Hill.
The third edition (ISBN 0-07-113540-5) p141 states:
"Sudorific glands are also known as sweat glands. Two types of suderic glands exist: eccrine and apocrine... The female breast contains apocrine glands that have become adapted to secrete and release milk instead of sweat."