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Host defense mechanisms

This wide range of pharmacokinetic properties, along with thek ease of administration, broad spectmm antimicrobial activity, and noninterference with host-defense mechanisms is responsible for thek widespread use five decades after thek discovery. [Pg.463]

In both cases, a seeming virus stimulator (twinberry extract) and a virus inhibitor (tannic acid) operated in a more or less similar way in the cucumber-TMV system. They both affect the host defense mechanism against virus infection. The active component in twin-berry extract exhibits a mild and temporary interference, thus permitting virus to make further rounds of gain (ringlike patterns) while tannic acid produces a strong and permanent interference. [Pg.100]

Cross A, Asher L, Seguin M, Yuan L, Kelly N, Hammack C (1995) The importance of a hpopoly-sacchaiide-initiated, cytokine-mediated host defense mechanism in mice against extraintesti-nally invasive escheiichia coh. J Clin Invest 96(2) 676-686 Dahan A, van Dorp E, Smith T, Yassen A (2008) Morphine-6-glucuronide (M6G) for postoperative pain relief. Eur J Pain 12(4) 403-411... [Pg.349]

The selective stimulation of these cells is of importance because they are the most active effector cells in host defense mechanisms against bacterial and viral infections. [Pg.684]

Older individuals have decreased host defense mechanisms such as slowed gastric emptying and decreased saliva production. They may present with atypical symptoms such as chest pain, asthma, hoarseness, coughing, wheezing, or poor dentition. These patients often do not seek medical attention because they believe their symptoms are part of the normal aging process. [Pg.266]

The first is glycosaminoglycan, a compound produced by the body that coats the epithelial cells of the bladder. This compound essentially separates the bladder from the urine by forming a protective layer against bacterial adhesion.14 A second compound known as Tamm-Horsfall protein is secreted into the urine, and prevents E. coli from binding to receptors present on the surface of the bladder. Other factors implicated in contributing to host defense mechanisms include immunoglobulins, specifically IgA, and lactobacilli, bacteria that are part of the normal vaginal flora.13,15... [Pg.1153]

Polyanionic polymers can enter into biological functions by distribution throughout the host and they behave similar to proteins, glycoproteins and polynucleotides which modulate a number of biological responses related to the host defense mechanism. These are enhanced immune responses, and activation of the reticuloendothelial system (RES) macrophages. [Pg.10]

Dystrophic neurites show decreased spine density and decreased spine stabilization with increasing proximity to the plaque core [20]. Ca2+-sensi-tive dyes reveal a profound elevation in Ca2+ in neurites that are closer to the plaque core [21]. The cause of this Ca2+ dysregulation is unknown, but it is interesting that host defense mechanisms associated with NPs,... [Pg.320]

Roily and Liebermeister [95] showed that bacteria introduced into the small bowel disappeared rapidly, without bile, pancreatic, and intestinal juices having antibacterial properties alone or mixed. Later studies, of which those by Dack and Petran [96], Dixon [99] and Dixon and Paulley [100] are of particular importance, provided considerable further evidence that intestinal peristalsis is the main line of defense against bacterial colonization of the small bowel. This was also concluded by Donaldson [101-103] when he reviewed host defense mechanisms in 1964. At that time, however, the insights into small bowel motility were confined to the reflex-mediated peristaltic behavior. [Pg.11]

Three factors determine the development of UTI the size of the inoculum, virulence of the microorganism, and competency of the natural host defense mechanisms. [Pg.557]

Jerrels, T.R., Saad A.J., and Domiati-Saad, R., Effects of ethanol on parameters of cellular immunity and host defense mechanisms to infectious agents, Alcohol, 9, 459, 1992. [Pg.540]

The ability of mast cells to promote and even to shape acquired immune responses was further corroborated by Maurer et al. [14] investigating host defense mechanisms in Leishmania major... [Pg.60]

The methylation of DNA at CpG islands has also turned out to be an important regulator for cell development, the differentiated proteome and the regulation of cell survival [237,238]. Indeed the implications of this chemical modification have been linked to DNA accessibility, chromatin fluidity and cell transformation [239,240]. DNA methylation is required for genomic stability and believed to act as an inert epigenetic marker in germinal cells and preimplantation embryos [238]. Presumably, DNA methylation is required for the heritable transmission of chromatin structure, which prevents the expression of terminally silenced genes in differentiated tissues, and provides a host-defense mechanism against parasitic transposable elements [241]. [Pg.259]

Infections Corticosteroids may mask signs of infection, and new infections may appear during their use. There may be decreased resistance and inability of the host defense mechanisms to prevent dissemination of the infection. Restrict use in active tuberculosis to cases of fulminating or disseminated disease in which the corticosteroid is used for disease management with appropriate chemotherapy. Corticosteroids may exacerbate systemic fungal infections and may activate latent amebiasis. [Pg.262]

Di Poto, A., Sbarra, M. S., Provenza, G., Visai, L., and Speziale, P. (2009). The effect of photodjmamic treatment combined with antibiotic action or host defense mechanisms on Staphylococcus aureus biofilms. Biomaterials 30(18), 3158-3166. [Pg.145]

Diethylcarbamazine immobilizes microfilariae and alters their surface structure, displacing them from tissues and making them more susceptible to destruction by host defense mechanisms. The mode of action against adult worms is unknown. [Pg.1149]

The three molecules of the IL-1 family, interleukin-la (IL-la), interleukin-1 3 (IL-ip), and interleukin-1 receptor antagonist (IL-IRa) map to the long arm of chromosome two in the human genome. It appears that the family arose via a gene duplication event some 350 million years ago, and the molecules possess between 27.5 and 36% sequence identity with each other (Table 2) [1,14,15]. In addition, the genes for the two IL-1 receptors IL-1R1 and IL-1RII [16,17], and an IL-1R accessory protein (IL-lRacP), which binds to the IL-1, IL-1 receptor complex [18], have been identified. Together, these molecules via their differential activity serve primarily to modulate the host defense mechanism. [Pg.398]


See other pages where Host defense mechanisms is mentioned: [Pg.34]    [Pg.497]    [Pg.34]    [Pg.325]    [Pg.434]    [Pg.365]    [Pg.431]    [Pg.1153]    [Pg.1153]    [Pg.555]    [Pg.56]    [Pg.152]    [Pg.75]    [Pg.190]    [Pg.238]    [Pg.50]    [Pg.309]    [Pg.16]    [Pg.87]    [Pg.178]    [Pg.422]    [Pg.433]    [Pg.31]    [Pg.50]    [Pg.368]    [Pg.34]    [Pg.559]    [Pg.658]    [Pg.659]   
See also in sourсe #XX -- [ Pg.660 ]




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