Page 841 - Veterinary Immunology, 10th Edition
P. 841

Although many bacteria are destroyed by phagocytosis, others
  VetBooks.ir  are killed when free in the circulation. Bacteria can be destroyed by

               complement acting through the alternate or lectin pathways.
               Bacterial cell walls, lacking sialic acid, inactivate FH and stabilize

               the alternate C3 convertase (C3bBbP). As a result, these bacteria are
               either opsonized or lysed. Activation leads to production of
               terminal complement complexes (TCCs). These TCCs alone may be
               unable to insert themselves into the carbohydrates of the microbial

               cell wall. However, lysozyme in the blood may digest the cell wall
               and enable the TCCs to insert themselves into the lipid bilayer of
               the inner bacterial membrane.
                  Antimicrobial peptides are critical for the defense against bacteria

               such as the mycobacteria (Box 26.1). Pulmonary collectins and
               surfactant proteins play an important role against Mycobacterium
               avium infections in the lung. They probably act by binding to, and
               agglutinating and opsonizing the bacteria. Suppression of bacterial

               growth by withholding iron is discussed in Chapter 7.



                 Box 26.1

               Vitamin D and Immunity


               When an intracellular bacterium such as Mycobacterium tuberculosis
               interacts with TLR1 or TLR2 on the surface of macrophages, it
               upregulates many different genes and enhances their antimicrobial
               activity. In mice, this is mainly mediated by nitric oxide. In
               humans, however, nitric oxide is not elevated, and other

               mechanisms are involved (Fig. 26.1). One gene activated by TLR1/2
               signaling in humans is that encoding the vitamin D receptor. This
               receptor is therefore upregulated on activated macrophages.

               Binding of vitamin D to its receptor upregulates expression of the
               gene for the antibacterial peptide cathelicidin. The cathelicidin, in
               turn, can kill intracellular M. tuberculosis. It is no coincidence,
               therefore, that resistance to tuberculosis is directly related to serum
               vitamin D levels and that humans with a deficiency of vitamin D

               show significantly decreased resistance to this infection. It is of
               interest to recall that sanatorium treatment of tuberculosis
               classically involved exposure to fresh air and sunlight, a procedure

               that would be expected to increase vitamin D levels in human




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