Background Chronic obstructive pulmonary disease (COPD) is a major public health problem associated with long-term exposure to toxic gases and particles. We examined the evolution of the pathological effects of airway obstruction in patients with COPD. Methods The small airways were assessed in surgically resected lung tissue from 159 patients — 39 with stage 0 (at risk), 39 with stage 1, 22 with stage 2, 16 with stage 3, and 43 with stage 4 (very severe) COPD, according to the classification of the Global Initiative for Chronic Obstructive Lung Disease (GOLD). Results The progression of COPD was strongly associated with an increase in the volume of tissue in the wall (P<0.001) and the accumulation of inflammatory mucous exudates in the lumen (P<0.001) of the small airways. The percentage of the airways that contained polymorphonuclear neutrophils (P<0.001), macrophages (P<0.001), CD4 cells (P=0.02), CD8 cells (P=0.038), B cells (P<0.001), and lymphoid aggregates containing follicles (P=0.003) and the abs...

/pdf/the-nature-of-small-airway-obstruction-in-chronic-5126v6d6li.pdf

The Nature of Small-Airway Obstruction in Chronic Obstructive Pulmonary Disease

Social support has been reliably related to lower rates of morbidity and mortality. An important issue concerns the physiological mechanisms by which support influences such health endpoints. In this review, I examine evidence linking social support to changes in cardiovascular, neuroendocrine, and immune function. Consistent with epidemiological evidence, social support appears to be related to more positive “biological profiles” across these disease-relevant systems. Recent research on immune-mediated inflammatory processes is also starting to provide data on more integrative physiological mechanisms potentially linking social support to health. The implications of these links, along with future research directions are discussed.

/pdf/social-support-and-health-a-review-of-physiological-1b1l84sy5u.pdf

Social Support and Health: A Review of Physiological Processes Potentially Underlying Links to Disease Outcomes

Plasmid DNAs expressing influenza virus hemagglutinin glycoproteins have been tested for their ability to raise protective immunity against lethal influenza challenges of the same subtype. In trials using two inoculations of from 50 to 300 micrograms of purified DNA in saline, 67-95% of test mice and 25-63% of test chickens have been protected against a lethal influenza challenge. Parenteral routes of inoculation that achieved good protection included intramuscular and intravenous injections. Successful mucosal routes of vaccination included DNA drops administered to the nares or trachea. By far the most efficient DNA immunizations were achieved by using a gene gun to deliver DNA-coated gold beads to the epidermis. In mice, 95% protection was achieved by two immunizations with beads loaded with as little as 0.4 micrograms of DNA. The breadth of routes supporting successful DNA immunizations, coupled with the very small amounts of DNA required for gene-gun immunizations, highlight the potential of this remarkably simple technique for the development of subunit vaccines.

https://www.pnas.org/content/pnas/90/24/11478.full.pdf

DNA vaccines: protective immunizations by parenteral, mucosal, and gene-gun inoculations

https://www.thelancet.com/pdfs/journals/lancet/PIIS0140-6736(04)16900-6.pdf

Pathophysiology of airflow limitation in chronic obstructive pulmonary disease

The early colocalization of T cells and the potent immunostimulatory cytokine IFN-gamma to atherosclerotic lesions suggest that the immune system contributes to atherogenesis. Since mice with a targeted disruption of the apoE gene (apoE 0 mice) develop profound atherosclerosis, we examined the role of IFN-gamma in this process. First, the presence of CD4(+) and CD8(+) cells, which secrete lesional IFN-gamma, was documented in apoE 0 atheromata. Then, the apoE 0 mice were crossed with IFN-gamma receptor (IFNgammaR) 0 mice to generate apoE 0/IFNgammaR 0 mice. Compared to the apoE 0 mice, the compound knock-out mice exhibited a substantial reduction in atherosclerotic lesion size, a 60% reduction in lesion lipid accumulation, a decrease in lesion cellularity, but a marked increase in lesion collagen content. Evaluation of the plasma lipoproteins showed that the compound knockout mice had a marked increase in potentially atheroprotective phospholipid/apoA-IV rich particles as well. This correlated with an induction of hepatic apoA-IV transcripts. These observations suggest that IFN-gamma promotes and modifies atherosclerosis through both local effects in the arterial wall as well as a systemic effect on plasma lipoproteins. Therefore, therapeutic inhibition of IFN-gamma signaling may lead to the formation of more lipid-poor and stable atheromata.

/pdf/ifn-gamma-potentiates-atherosclerosis-in-apoe-knock-out-mice-2urzqkdeyk.pdf

IFN-gamma potentiates atherosclerosis in ApoE knock-out mice.

Cellular and molecular immunology , Cellular and molecular immunology , کتابخانه الکترونیک و دیجیتال - آذرسا

Cellular and Molecular Immunology

B cell activation and antibody production

Immunity to tumors

Properties and overview of immune responses

128 The specialized immune mechanisms that function to eradicate intracellular microbes constitute cellmediated immunity. The effector phase of cellmediated immunity is carried out by T lymphocytes, and antibodies play no role in eradicating infections by microbes that are living inside host cells. The phases of cell-mediated immunity consist of the activation of naive T cells to proliferate and to differentiate into effector cells and the elimination of cell-associated microbes by the actions of these effector T cells. In Chapter 3 we described the function of major histocompatibility complex (MHC) molecules in displaying the antigens of intracellular microbes for recognition by T lymphocytes, and in Chapter 5 we discussed the way in which naive T cells recognize these antigens in lymphoid organs and develop into effector cells. In this chapter, we will address the following questions: • How do effector T lymphocytes locate intracellular microbes at any site in the body? • How do effector T cells eradicate infections by these microbes?

Shiv Pillai

Papers

Cellular and Molecular Immunology

B cell activation and antibody production

Immunity to tumors

Properties and overview of immune responses

Effector mechanisms of cell-mediated immunity