[Meningoencephalitis by Listeria in the lupus disease]. / Meningoencefalitis por Listeria en el lupus.

We present a patient with lupus nephropathy of 20 years of evolution in treatment with oral steroids who developed a meningoencephalitis associated to bacteraemia by Listeria monocytogenes. The patient was treated successfully with gentamicin and ampicillin for 6 weeks. Infection by Listeria monocytogenes occurs more frequently in individuals with some form of immunodeficiency like lupus disease, with a mortality around 30%.

Effect of cyclosporin A on inflammatory cytokine production by human alveolar macrophages.

Cyclosporin A (CsA) is an immunomodulator drug that has been used in the treatment of several types of advanced pulmonary interstitial disease. This beneficial effect occurs mainly in circumstances in which alveolitis due to CD4 lymphocytes is absent, suggesting that CsA acts on other types of cells. The present study was undertaken to determine the effect of CsA on inflammatory cytokine secretion by human alveolar macrophages (AMs). Human AMs were collected by bronchoalveolar lavage from four control subjects and 13 patients with interstitial lung disease. Purified human AMs were incubated with different concentrations of CsA (200, 20 and 2 ng ml-1) in the presence or absence of lipopolysaccharide (LPS). Interleukin-1 beta (IL-1 beta), tumour necrosis factor-alpha (TNF-alpha), IL-6 and IL-8 levels were measured in supernatants using specific enzyme-linked immunosorbent assays. It was found that CsA inhibits basal secretion of TNF-alpha and IL-8 at 20 and 200 ng ml-1. However, none of the different concentrations of CsA modified basal secretion of IL-1 beta nor IL-6. By contrast, a lower concentration of CsA (2 ng ml-1) inhibits LPS-stimulated secretion of all inflammatory cytokines. It is concluded that CsA exerts a modest effect on inflammatory cytokine production by human AMs.

Action of cyclosporin A on mononuclear phagocytes.

Classically, cyclosporin A has been reported to exert its immunomodulatory action through its effect on T lymphocytes by inhibiting the synthesis of interleukin 2. However, the inhibition of T-lymphocyte activation does not suitably account for all the effects observed following cyclosporin A administration. It is possible that some of them could be due to the action of cyclosporin A on other cells, among which are mononuclear phagocytes. This article offers a detailed review of the consequences of the interaction of cyclosporin A on the capacities (surface antigen expression and production of inflammatory mediators), functions (chemotaxis, phagocytosis, intracellular destruction and cytotoxicity) and actions (antimicrobial defense, antitumor defense and immune cooperation) of these cells. The general conclusion is that the capacities, functions and actions of the macrophages related to non-specific defense are more resistant to cyclosporin A than those related to immunoregulation.

[Acute eosinophilic pneumonia in a pregnant woman]. / Neumonía eosinófila aguda en gestante.

Acute eosinophilic pneumonia is a recently described pulmonary phenomenon involving rapidly progressing respiratory insufficiency. Although it can appear at any age, it has never been reported during pregnancy and its impact on gestation is therefore unknown. We describe the clinical signs and course of disease in this first report of acute eosinophilic pneumonia in a pregnant woman. We emphasize the diagnostic utility of bronchoalveolar lavage, the resolution of symptoms without corticoid treatment and, mainly, the absence of adverse repercussions of the disease on pregnancy.

[Septic shock and multiple organ failure caused by Mycobacterium tuberculosis]. / Shock séptico y fallo multiorgánico por Mycobacterium tuberculosis.

We report a case of death from septic shock with multiorganic failure of tuberculosis origin. We described, the pathogenic mechanism of the sepsis and respiratory distress due to Mycobacterium tuberculosis. Another aspect of interest was the hemodynamic demonstration of septic shock due to M. tuberculosis.