Scientific journal

European Journal of Natural History

ISSN 2073-4972

ИФ РИНЦ = 0,301

The smoking factor as negative trigger unites a number of bronchopulmonary diseases and first of all chronic obstructive pulmonary disease (COPD) and LC as cancer is almost always developed with long term smokers with COPD. That´s why it is seen rational to research clinical-immunological differences and similarities COPD and LC as diseases developing on the basis of common target tissue: LC and COPD are diseases with etiologically significant environmental factors.

There is a lot of data confirming the role of chronical inflammation in cancer genesis generally and LC in particular (Baron et Sandler, 2000; Garcia-Rodriguez LA, Huerta-Alvarez C, 2001). It is proved that proliferative and cancerous tissue transformation and also chronical inflammation are dependent on the level of immune alterations, are provided by system alterations of immunocompetent cells, their relations on different levels of pathologic process (Paltsev M.A., Ivanov A.A., 2003; Shvartsburd P.M./ 2006; Macarthur et al., 2004)

It is adjusted that there is estimated cancerous potential when there´re different disregenerated changes of lung epithelia against chronical inflammatory lung disease (Kogan E.A., 2003). This is explanation of a fact of often developing cancer against COPD when dysplastic changes and metaplasia of bronchial epithelia are clinical implications.

It´s important to mark that the appearance of chronical inflammatory in bronchopulmonary tract with dominating concentration of CD 8+ lymphocytes, neutrophils, macrophages is typical for COPD. Moreover it is typical for COPD clinical accompaniment in the form of progressive bronchial obstruction against anatomical airways remodeling (Jeffery P.K., 2001).

Despite the known fact of COPD and LC development with heavy smokers, till now

there are just singular facts in scientific literature pointing at association of COPD with high risk formation of LC (Kishi K. et al., 2002; Mannino M.D.et al., 2004).

The objective of the research is a clinical-immunological estimate of COPD patients, including those with LC formation.

Materials and methods

Clinical-immunological examination is done for 30 patients with COPD medium severity level and 30 patients with COPD medium severity level with clinical- roentgenologic and histologically confirmed LC in the period from February to May 2009. Male patients aged 40-60 years old with average smoking experience- 20 years are included in the research.

Control group for laboratory research included 24 almost healthy men - volunteers aged 40-60 years old.

There were detected content of main population and subpopulation of lymphocyte(CD3+CD16-, CD3+CD4+, CD3+CD8+, CD4+/ CD8+, CD19+, CD3-CD16+, CD3+CD16+, CD3-CD8+, CD4+CD25+, CD25+ CD4+95+, CD95+, CD4+HLADR+, HLADR+, CD19+CD23+) according to method of ductal cytofluorometry by using monoclonal antibodies, phagocytic activity of neutrophils with cell ability to absorb latex elements and level of B-cell stimulatory factor 2(BSF-2) in blood serum.

Research results

It is known that T-lymphocytes initiate and regulate immune response, perceive antigens, which in their turn influence their activity and population increase. Content of T-lymphocytes in blood is instable an depends on body state (stress, chronic or acute inflammation) (Hodge S.J. et al., 2003).

Characteristics of some immunologic parameters with patients with chronic obstructive pulmonary disease are presented in table 1.

*- differences are true in comparison with control group (*-р<0,01; ** - р<0,05).

Interpreting results from table 1, which include the most changed immunological markers with COPD patients, the following is marked.

CD16+ is membrane antigen of natural killer (NK). Their unique peculiarity- is the ability to spontaneously, without antigen presensitization, kill virus-infected, oncotic and other types of changed cells. It is also known that antigen activation of T-cells leads to interleukin-2 production increase and expression of its receptions on cell surface. It may be a sign of T-lymphocyte activation and their preparation to proliferation. Receptions to interleukin-2, expressed mainly at activated T-lymphocyte surface is characterized as CD25+ - antigens (Kubysheva N.I. etc., 2007)

Our results show simultaneous growth of CD16+ and CD25+-antigen (p<0.01), that may show the development of hyperergic immune response influenced by external action.

CD95+ -anigen (Fas) is a cell reception triggering apoptosis (Krueger A. et al., 2003). CD95 - ligand (Fasl) mediate the death of cells sensitive to apoptosis by connecting with CD95+ -anigen. CD95 - ligand is presented in exess on activated Т (CD8+ and CD4+) - and В - lymphocytes, NK, lung cells (Ricci - Vitiani L. et al., 2000).

As a part of the study we´ve discovered tendency to cell number growth, expressing CD95+ - antigen (p<0.01).

Apoptosis, being a physiological form of cell death, plays key role in inflammation resolution. High apoptosis of activated T-cells may lead to homeostasis imbalance, leading to overload of local ability of phagocytes and defective clearance. According to Hodge and co-authors (2003), this may potentially lead to saving apoptosis material, additional alteration and inflammation progression. Thus, growth of CD95+-mononuclear with obstructive pulmonary disease may show inflammation progression and correspondingly unfavorable disease.

Phagocytic index (neutrophil percentage, taking part in phagocytosis) is also increased in comparison to control group. Phagocytosis- is an important component of antibacterial defense. Initial defense reaction to any infection depends on recognition of general components for different germs with the help of special cell receptors, which differ from antigen-specific receptors T- and B- cells. Numerous components of germ cells may cause phagocyte chemotaxis in the centre of infection (Roitt A. etc., 2000).

Our research has also shown the growth of BCF2 in blood serum. BCF2 is pro- and antiflammotory delirient, which is the main activator of synthesis of protein of acute phase hepatocyte; it helps involving kidney mesangial cells into inflammatory process, B- and T- lymphocytes and takes part in proliferation induction of the least (especially in the case of B-cells and plasmocytes); acts upon hematopoiesis stimulating its early stages; upon neuroendocrinal system; helps developing fever and adrenocorticotropic hormone secretion. Moreover it suppresses production of interleukin-1, tumor necrosis factor-α and prostaglandin E2 with macrophage, by that helping accomplishment of inflammatory reaction. Stimulatin production of adrenocorticotropic hormone, BCF2 takes part in development of stress reactions also connected with inhibitory action glucocorticoids (Yarilin A.A., 1999).

Thus COPD and LC have the same characteristics of chronic inflammatory process, in formation of which, probably, other components of inflammatory cascade.

Taking into consideration commonality of the participant pathologic process - target tissue, presence of common markers, reacting more significantly (CD3- CD16+, CD4+CD25+, CD95+, HLA -DR+, Phagocytic index, BCF2), the obtained data can be considered as the proof of pathogenetic commonality of COPD and LC and consider them as stages of the same process. Moreover COPD can be considered premorbid stage of LC.

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The work was submitted to international scientific conference «Prospects for the development of university science», Dagomys (Sochi), September 21-24, 2009. Came to the editorial office on 30.07.2009.