Will nodules grow if both lungs are inflamed?

When some people go to the hospital for a check-up, they are often told that both lungs are inflamed. At this time, everyone begins to worry and doubt, fearing that nodules will appear in their lung function. When the condition is not clear and not thoroughly understood, don't worry. You must first undergo an examination to know the calm state at the moment.

Causes

1. Cause: Not yet clear. Infectious factors (such as bacteria, viruses, mycoplasma, fungi, etc.) have been observed, but no definite conclusion has been reached. Genetic factors have also been studied but have not been confirmed. In recent years, some authors have used PCR technology to find that the positive rate of Mycobacterium tuberculosis DNA in patients with sarcoidosis is as high as 50%. Therefore, they proposed that sarcoidosis is the result of mycobacteria invading tissues, but many experiments have not confirmed this argument.

Most people now believe that disorders of cellular immunity and humoral immunity are important pathogenesis of sarcoidosis. Under the stimulation of certain (certain) sarcoidosis-causing antigens, alveolar macrophages (Am) and T4 cells are activated. Activated Am releases interleukin-1 (IL-1), which is a very strong lymphokine that can stimulate lymphocytes to release IL-2, causing T4 cells to multiply and, under the action of lymphokines, activate B lymphocytes, release immunoglobulins, and cause hyperfunction of autoantibodies. Activated lymphocytes can release monocyte chemotactic factor, leukocyte inhibitory factor and macrophage migration inhibitory factor. Monocyte chemotactic factor causes monocytes in the peripheral blood to continuously gather in the alveolar interstitium. In sarcoidosis, its concentration in the alveoli is about 25 times that of the blood. Under the action of many unknown antigens and mediators, T lymphocytes, monocytes and macrophages infiltrate the alveoli, forming the early stage of sarcoidosis - the alveolitis stage.

As the lesion progresses, the cellular components of alveolitis continue to decrease, while the number of macrophage-derived epithelial cells gradually increases. Under the action of the granuloma-inciting factor (granuloma-inciting factor) synthesized and secreted by them, typical non-caseous sarcoidosis granulomas gradually form. In the later stage, fibronectin (Fn) released by macrophages can attract a large number of fibroblasts (Fb) and make them adhere to the extracellular matrix. In addition, the fibroblast growth factor (GFF) secreted by macrophages promotes the increase in the number of fibroblasts; at the same time, the surrounding inflammatory and immune cells further decrease and even disappear, leading to extensive pulmonary fibrosis.

Pathogenesis

Sarcoidosis is the result of the conflict between unknown antigens and the body's cellular and humoral immune functions. Due to individual differences (age, gender, race, genetic factors, hormones, HLA) and the regulation of antibody immune response, the development and regression of granulomas are determined by the imbalance between the promoting factors and antagonistic factors produced, showing different pathological states and natural remission trends of sarcoidosis.