Bacterial proteins, invasion

Recent work indicates that a major virulence mechanism for Salmonella may involve type III secretion systems, which are encoded on plasmids and allows direct transfer of bacterial proteins to eukaryotic cells through a contact-dependent secretion mechanism. These effector proteins are capable of enhancing virulence and epithelial cell invasion. 

Other adhesins of E. coli as antigen 43, AIDA-I, TibA and intimin of enter-opathogenic and enterohemorrhagic E. coli are true afimbrial adhesins i.e. they are integral outer membrane proteins. However, also intimin seems to be involved in invasion of host cells [62, 63], Intimin, which is actually a whole family of adhesins, is the only example of an adhesion that uses a protein (Tir translocated intimin receptor) in the host cell membrane, that is a bacterial protein inserted into the host by the bacterial type 3 protein secretion system [64],... 

Bacillus thuringiensis produces a variety of organic compounds which are toxic to the larvae of certain susceptible insect hosts. Among the toxic entities are proteinaceous crystals, probably three soluble toxins, and certain enzymes. The protein material is the major toxin active in killing lepidopterous larvae. The protein is formed by the cells apparently in close synchrony with sporulation, and its nature is a constant function of bacterial strain. The mode of action of the protein is under study. The sequence of events in the pathology observed is probably solubilization of the crystal (enzymatic or physical)—>liberation of toxic unit—>alteration of permeability of larval gut wall— change in hemolymph pH—>invasion of hemolymph by spores or vegetative cells of the bacterium. 

EPEC causes a degeneration of the microvillus brush border, with cupping and pedestal formation of the plasma membrane at the sites of bacterial attachment and reorganization of cytoskeletal proteins [43, 44], Invasion has been observed in some clinical specimens, but the mechanism of how this bacteria produces diarrhea is not fully understood. Some possibilities include an increase in permeability and loss in microvilli leading to malabsorption. 

Serious adverse events occur in up to 6% of patients with anti-TNF therapy. The most important adverse effect of these drugs is infection due to suppression of the ThI inflammatory response. This may lead to serious infections such as bacterial sepsis, tuberculosis, invasive fungal organisms, reactivation of hepatitis B, listeriosis, and other opportunistic infections. Reactivation of latent tuberculosis, with dissemination, has occurred. Before administering anti-TNF therapy, all patients must undergo purified protein derivative (PPD) testing prophylactic therapy for tuberculosis is warranted for patients with positive test results. More common but usually less serious infections include upper respiratory infections (sinusitis, bronchitis, and pneumonia) and cellulitis. The risk of serious infections is increased markedly in patients taking concomitant corticosteroids. 

MTMl (33). This molecule can be removed either by phosphorylation into P1-4,5-P2 by phosphorylation with the fS-form of P1-4K (34) or by dephosphorylation of P1-5-P by the novel form of PTEN-like proteins with selectivity toward phosphatidyh-nositol phosphorylated at the 5-position (35). Recent studies suggest a role for P1-5-P in a variety of cellular events, such as tumor suppression, response to bacterial invasion (35), and control of osmotic pressure (36). This phospholipid has been shown recently to function as a second messenger that binds to an Arabidopsis homolog of trithorax, which suggests that it may have a regulatory function that connects lipid signahng with nuclear functions (37). 

Necrotic phase This phase occurs 1-4 days after injury. Cells die from coagulation of intracellular protein. Vascular thrombosis and bacterial invasion may worsen the underlying injury. The esophagus is especially vulnerable to perforation during this phase. 

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