Asthma in the elderly (AIE) is under diagnosed and under treated and there is a paucity of knowledge. The National Institute on Aging convened this workshop to identify what is known, what gaps in knowledge remain and suggest research directions needed to improve the understanding and care of AIE. Asthma presenting at an advanced age often has similar clinical and physiologic consequences as seen with younger individuals but co-morbid illnesses and the psychosocial effects of aging may affect the diagnosis, clinical presentation and care of asthma in this population. At least two phenotypes exist among elderly asthma; those with long-standing asthma have more severe airflow limitation and less complete reversibility than those with late-onset asthma. Many challenges exist in the recognition and treatment of asthma in the elderly. Furthermore, the pathophysiological mechanisms of AIE are likely to be different from those seen in young asthmatics and these differences may influence the clinical course and outcomes of asthma in this population.

Cytomegalovirus (CMV) was cultured from the urine of 14 of 190 homosexual but none of 101 heterosexual men attending a venereal disease clinic (P less than 0.005). Viruria was confined to men less than 30 years of age and was present in 14% of this group. Antibody to CMV was measured in the sera of 139 homosexual and 70 heterosexual men attending the same clinic and in 103 male volunteer blood donors. Titers were found in 94% of homosexual patients but in only 54% of heterosexual patients (P less than 0.005) and 43% of male volunteer blood donors (P less than 0.005). The data suggest that sexual transmission is an important mode of spread of CMV among adults and the homosexual men are at greater risk for CMV infections than are heterosexual men. Homosexual men might considered candidates for the evaluation of the efficacy of CMV vaccines in preventing horizontal transmission of infection.

Matrix metalloproteinases (MMPs) modulate development, inflammation, and repair in lungs. Tissue inhibitors of MMPs (TIMPs) interact with MMPs, controlling the intensity and nature of the response to injury. Absence of MMP-9, -2, and -8 activities is associated with altered lung inflammation during allergic sensitization. To test the hypothesis that the absence of TIMP-1 enhances allergic lung inflammation, airway hyperreactivity (AHR), and lung remodeling in asthma, we studied TIMP-1 null (TIMP-1 KO) mice and their WT controls using an ovalbumin (OVA) asthma model. TIMP-1 KO mice, compared to WT controls, developed an asthma phenotype characterized by AHR, pronounced cellular lung infiltrates, greater reduction in lung compliance, enhanced Th2 cytokine mRNA and protein expression, and altered collagen lung content associated with enhanced MMP-9 activity. Our findings support the hypothesis that TIMP-1 plays a protective role by preventing AHR and modulating inflammation, remodeling, and cytokine expression in an animal model of asthma.