Non-Hodgkin’s lymphoma in the course of asthma – incidence or predisposition?

Asthma is a chronic inflammatory disease of the respiratory tract. Inflammation is induced by mediators released by the plurality of cells of the immune system. In this process, the main role is played by cytokines such as interleukin-25 (IL-25) [1–7] and mast cells that, by the excretion of a number of cytokines, induce bronchospasm [6, 7]. The diagnosis of asthma is still based on clinical symptoms and spirometry test. Approx. 80% of patients with asthma develop rhinitis that is the ordinary inflammation of the upper respiratory tract [2, 3, 6]. This confirms the involvement of the entire respiratory tract in the mucosal inflammatory process. Non-Hodgkin’s lymphoma (NHL) is a cancer of the lymphoid system. The most common symptoms include swollen lymph nodes and/or the extralymphatic presence of a tumour, and generalised symptoms like fever, night sweats, or weight loss [8] and the enlargement of the spleen or liver, abdominal pain, or dyspeptic symptoms. A significant splenomegaly is usually related to anaemia, thrombocytopaenia, or leukopaenia. Most patients with NHL reveal impaired immunity from the beginning of the disease, and treatment (especially chemotherapy and immunotherapy) intensifies this condition. The impairment of the humoral and cellular immunity in NHL patients predispose to increased morbidity for atypical infections [8–10]. Tumor necrosis factor  (TNF-), tumour necrosis factor is a homotrimer formed as an integral membrane protein, which, under specific metalloproteinase TACE (TNF- converting enzyme), is released from the cell. It is produced by many cells: monocytes, macrophages, and lymphocytes. The strongest factor stimulating its release is the lipopolysaccharide component of the bacterial membrane. Practically all nucleated cells contain the receptors for TNF- on their surface, hence its differential effects [4]. Interleukin-25 belongs to the family of cytokines of the IL-17 group showing the pleiotropic mechanism of action via receptor IL-17RB. Its other (older) name is IL-17E. Interleukin-25 is secreted by Th2 helper cells and mast cells; it inhibits production of IL-1 and IL-23 [4] but induces the release of other cytokines like IL-4, IL-5, IL-13, and eotaxin [4]. This stimulates eosinophils and production of IgE antibodies associated with the development of allergy. Interleukin-25 facilitates the process of diapedesis of neutrophils, which are an important factor in the development of severe asthma. It is already known...


View full text...