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Cellular Communication and Signal Transduction Associated With Infectious Diseases and Toxins


In humans, cellular communication is accomplished through various types of signaling molecules. Several mechanisms exist for transmitting a message from one cell to another for the continuation of homeostasis within the body. These cellular communications can be either short distance known as the paracrine or long distance through endocrine system. Importantly, cellular communications in the brain is accomplished through signaling transduction molecules known as neurotransmitters.

It is important to keep in mind that infectious agents responsible by infectious diseases are recognized as foreign substances upon their entry into human systems or cells. As such, both the innate and adaptive immune system of human body exerts a pressure on the infectious organisms either phagocytizing them or killing them through the humoral immune system. All these processes are mediated through cellular communication involving signaling molecules.

The pathogenic microorganism first effort is to manipulate the host cellular communication and signaling mechanisms, so their presence within the human body is unnoticed. The pathogens secrete several virulence factors providing hiding advantage from the host machinery. Some of these virulence factors mainly accomplish this through their effect on the cellular communication mechanism.

Importantly host cellular communication targets by the infectious organisms are enzymes mediating cellular communication and signaling transduction mechanisms like GTPases, and kinases involved in cellular communications and molecular trafficking within and outside the cell.

Several bacterial toxins like Cholera toxin produced by Vibrio cholera and Pertussis toxin produced by the Bordetella pertussis mainly exert their toxic effect through damaging the cellular communication mechanisms. Importantly, the Cholera Toxin elevate the levels of cyclic AMP leading to efflux of chloride ions and water the primary cause of diarrhea, whereas the Pertussis toxin causing whooping cough hinders the G protein signaling for inflicting the diseases.

Viral infection mainly the oncoviruses (cancer causing viruses) are notorious for disabling the cellular communication and signaling machinery. The Rous Sarcoma Virus (RSV) mediated tumorigenicity in the chicken model were the earlier observation showing how the viral proteins can affect the Ras signaling involved in cellular communication in the eukaryotic cells ultimately shedding light on their pathogenic potentials through subverting the communication mechanisms. There are numerous examples relevant to the viral infections associated disruption of cell communications.

Besides disrupting the communication, the infectious agents are also involved in facilitating the infection process through tilting the cell communication support in favor of pathogens entry into the human cells. A detail of various mechanisms and molecular moieties involved is available in several articles delineating this topic [1-3].

Like bacterial and viral infections, the fungal infections, as well as parasites, are supposed to disrupt cellular communication machinery, either through blocking the cell messengers through occupying the cellular surfaces or secreting certain deleterious compounds.

Particularly, for toxins impact on the cell communication each and every toxin has its individualized impact on cell communications. A brief about the bacterial toxins have been provided as above. Importantly, neurotoxins inhibit the nerve transmission by inhibiting the activity of chemicals involved in nerve cell communication processes. For example inhibition of acetylcholinesterase by certain neurotoxins curtail the synthesis of acetylcholine involved in neuronal cell communications the ultimate cause for several neurological ailments [4].

1. Alto, N.M. and K. Orth, Subversion of cell signaling by pathogens. Cold Spring Harb Perspect Biol, 2012. 4(9): p. a006114.;
2. Bhavsar, A.P., J.A. Guttman, and B.B. Finlay, Manipulation of host-cell pathways by bacterial pathogens. Nature, 2007. 449(7164): p. 827-34.;
3. Shames, S.R., S.D. Auweter, and B.B. Finlay, Co-evolution and exploitation of host cell signaling pathways by bacterial pathogens. Int J Biochem Cell Biol, 2009. 41(2): p. 380-9.
4. Huang, Q., et al., Visible-light-activated photoelectrochemical biosensor for the study of acetylcholinesterase inhibition induced by endogenous neurotoxins. Biosens Bioelectron, 2013. 45: p. 292-9.

Topics: Infectious Diseases

Professor Dr. Muhammad Mukhtar

Written by Professor Dr. Muhammad Mukhtar

Professor Dr. Muhammad Mukhtar has over 25 years teaching experience in biomedical sciences. Besides teaching, he has a very strong portfolio of academic administration and he is an accomplished researcher in the area of infectious diseases. Dr. Mukhtar received his Ph.D. in Biosciences from the Drexel University of Philadelphia, USA, and also completed a Graduate Certificate in Research Management from Thomas Jefferson University of Philadelphia, USA. He served in various academic/administrative positions in the USA on an outstanding scientist (O-1) visa.