Although changes in T lymphocyte subset distribution in the peripheral blood of patients infected with human immunodeficiency virus (HIV) controls).The ratio of duodenal to circulating CD4+ T cells was significantly reduced to 0.2 (0-1) in AIDS patients (p<0-001) and even to 0.1 (0.04-0.5) in asymptomatic HIV infected patients (p<0.002) compared with 0.72 (0.44-0.95) in controls. These findings show an early and preferential loss of duodenal CD4 T cells in HIV infection. Immunological abnormalities in HIV infection are distinct between lymphoid compartments, and profound immunodeficiency may occur in the intestinal immune system although circulating T celis are largely preserved. (Gut 1995; 37: 524-529)

General features. Haemangiomas are benign vascular tumours. They can regress spontaneously as a result of fibrosclerosis, suggesting a conservative approach wherever possible. Asymptomatic haemangiomas do not require treatment. Renal haemangioma. In all, 198 cases have been reported. The lesion is usually solitary and unilateral and occurs most often in the pyramid, and in the mucosa or subepithelial tissue of the pelvis. In some cases a tentative diagnosis of haemangioma has been made by means of selective renal angiography and pre- or per-operative renoscopy. Partial nephrectomy is recommended in cases of minor haemangioma. Ureteric haemangioma. Six cases have been described. When haemangioma is suspected a conservative operation is recommended. Bladder haemangioma. A total of 106 cases have been reported. Many of the tumours had the characteristics of an iceberg, with considerable extravesical extension making endoscopic management less suitable because of the possibility of massive haemorrhage or recurrence. Consequently, many authors prefer local excision. In the case of endoscopic treatment the patient should be prepared for open surgery. Urethral haemangioma. Twenty cases have been described. The lesions often extend further than is immediately apparent. Endoscopic management is recommended for small lesions and, in the case of more extensive lesions, open exploration is advised followed by appropriate urethral reconstruction.

The activation of primary human airway epithelial cells (HAECs) and of the bronchial epithelial cell line BEAS-2B by Chlamydia pneumoniae, an important respiratory pathogen, was characterized. A time-dependent enhanced release of interleukin (IL)-8 and prostaglandin-E(2) and an increased expression of the epithelial adhesion molecule intercellular adhesion molecule-1 (ICAM-1), followed by subsequent transepithelial migration of polymorphonuclear neutrophils (PMN), were also demonstrated. The transepithelial PMN migration could be blocked by an anti-ICAM-1 monoclonal antibody (MAb) but not by MAbs against IL-8. In addition, there was an enhanced C. pneumoniae-mediated activation of NF-kappaB within 30-60 min in HAECs and BEAS-2B, which was followed by increases in mRNA synthesis of IL-8, ICAM-1, and cyclooxygenase-2, with maximal effects occurring 2 h after infection. Thus, C. pneumoniae infects and activates HAECs and BEAS-2B and therefore may be able to trigger a cascade of pro- and anti-inflammatory reactions during chlamydial infections.

Epithelial cells actively participate in inflammatory airway disease by liberating mediators such as arachidonate metabolites and cytokines. Inhibition of phosphodiesterases (PDEs) may be a useful anti-inflammatory approach. The PDE isoenzyme pattern and the effects of PDE inhibition on mediator generation were analyzed in primary cultures of human and porcine airway epithelial cells (AEC) and in the bronchial epithelial cell line BEAS-2B. PDE4 and PDE5 were detected in lysates of all cell types studied. In primary cultures of human AEC, the PDE4 variants PDE4A5, PDE4C1, PDE4D2, and PDE4D3 were identified by polymerase chain reaction analysis. Evidence of the recently described PDE7 was obtained by rolipram- insensitive cyclic adenosine monophosphate (cAMP) degradation, and its presence was verified by the demonstration of PDE7 messenger RNA. Primary cultures of human airway epithelium also expressed PDE1. Enhanced epithelial cAMP levels, induced by forskolin and PDE4 inhibition, increased formation of prostaglandin E2 (PGE2), but not of interleukin (IL)-8 or 15-hydroxyeicosatetraenoic acid (15-HETE) in airway epithelial cells. Increased cyclic guanosine monophosphate levels in these cells provoked by sodium nitroprusside and the PDE5 inhibitor zaprinast reduced the PGE2 synthesis, whereas 15-HETE and IL-8 formation were unchanged. The data suggest that PDE isoenzymes are important in airway inflammation and that PDE inhibitors exert anti-inflammatory effects by acting on AEC.