The extremes of life represent periods of high health risks. We recognize that a number of factors create these 2 troublesome risk periods—developing or declining immune systems, close contact and crowding in daycare or eldercare, and critical organs that either haven’t reached their prime or have passed it. In their recent paper on pneumococcal pneumonia
, Birjandi and Witte indicate, “Infection with pneumococcal pneumonia has been most successfully overcome in children, but it is still a problem in the elderly, particularly community-living older individuals.”
In this insightful summary, the authors indicate that the differences between the very young and the very old have been difficult to sequester. In both groups, the lungs have built-in ‘checkpoints’ to control pathogenic pneumococcal infection—checkpoint mechanism restrict colonization to upper airways, suppress invasive strains, and can rapidly engage innate immune responses of alveolar epithelia, macrophages and neutrophils if necessary.
Why, then, are the elderly at greater risk than young children?
They propose that both groups have immunologic gaps against pathogenic bacteria, which trigger a subset of B lymphocytes called marginal zone (MZ) B cells located in the spleen. This response is T-cell-independent. In children, development of MZ B cells lags behind other immune cells, making them more susceptible to pnuemococal pneumonia.
In the senescent adult, less is known about MZ B cells. Elderly adults may be at increased riskfor pnuemococal pneumonia because of a premature demise in MZ B cells. They discuss a few known facts and possibilities:
After entering the lung, S. pneumoniae uses enters the host’s own receptor for platelet-activating factor to gain access to their blood.
Once in the bloodstream, the spleen filters S. pneumoniae by binding to the specialized marginal zone macrophages (MZMs).
Studies have demonstrated a healthy spleen’s importance for clearing pneumococcus by phagocytosis, showing that asplenic and hyposplenic individuals are less able to clear this organism than healthy others. Asplenic patients and hyposplenic individuals are difficult to vaccinate and have a decrease in IgM memory B cells after pneumococcus infection.
MZMs have specific cell surface receptors (SIGN-R1) for S. pneumonia; once the bacteria engage with the SIGN-R1, the spleen is able to produce anti-pneumococcal IgM antibodies.
Animal studies have shown that (1) SIGN-R-deficient animals are more susceptible to pneumococcal infection.
Although elders phagocytic function in individual MZM seems to be preserved, reduced numbers of MZMs and MZ B cells in the aged may be the specific cause for increased susceptibility.
They suggest future investigations should attempt to uncover reasons for MZM quantity decline, and determine if any intervention can replenish them.
Current vaccine therapies target T-independent responses to generate immunity against pneumococcus.