WORLD JOURNAL OF ADVANCE
HEALTHCARE RESEARCH

Bernard J., N. Marguerite, M. Inks, R. L. Cooper and Dr. Bhumija Trivedi*

ABSTRACT

Background and Objective: An initial action of bacterial sepsis from gram-negative bacterial is a result due to the presence of Lipopolysaccharide (LPS), a bacterial endotoxin, which triggers the release of proinflammatory cytokines. There is suggestive evidence from neuronal responses in Drosophila and mammals that the gram-negative bacterial endotoxin LPS binds to TRPA1 receptors, one type of thermal detectors. We examined if LPS activates or blocks TRPA1 receptors in motor neurons and muscle fibers. Materials and Methods: The TRPA1 receptors were overexpressed and blocked in expression, by RNAi expression, in muscle and motor neurons. The effect on synaptic transmission and direct effects on neurons and muscle fibers were examined electrophysiologically. Results: The responses of blocking glutamatergic postsynaptic receptors by LPS were preserved with activation of TRPA1. Activation of TRPA1 in muscle depolarized the muscle in the presence of LPS but less so than without LPS due to the hyperpolarizing effect by LPS. Expression of RNAi for TRPA1 blocked responses to thermal activation but not actions by LPS. Conclusion: LPS does not activate or block TRPA1 receptors in these studies. This study has implications in the mechanisms by which LPS functions in its direct action on cells for potentially mediating the action of LPS and the downstream activation of proinflammatory cytokines.

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