Defense Mechanisms and Immunology - PowerPoint PPT Presentation

Defense mechanisms and immunology
1 / 23

  • Uploaded on
  • Presentation posted in: General

Defense Mechanisms and Immunology. Pulmonary surface-active material (surfactant) allows one to breathe effortlessly. In the absence of surfactant, the work of breathing may increase from less than 2% to more than 10% of total oxygen consumption.

I am the owner, or an agent authorized to act on behalf of the owner, of the copyrighted work described.

Download Presentation

Defense Mechanisms and Immunology

An Image/Link below is provided (as is) to download presentation

Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author.While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server.

- - - - - - - - - - - - - - - - - - - - - - - - - - E N D - - - - - - - - - - - - - - - - - - - - - - - - - -

Presentation Transcript

Defense mechanisms and immunology

Defense Mechanisms and Immunology

Defense mechanisms and immunology

  • Pulmonary surface-active material (surfactant) allows one to breathe effortlessly.

  • In the absence of surfactant, the work of breathing may increase from less than 2% to more than 10% of total oxygen consumption.

Defense mechanisms and immunology

  • Surfactant provides the low surface tension at the air-liquid interface that is necessary to prevent atelectasis, alveolar flooding, and severe hypoxia.

  • surfactant is also important for maintaining the patency of small airways

Surfactant protein a

Surfactant Protein A

  • SP-A is not essential for normal metabolism and processing of surfactant in vivo

  • The major function of SP-A appears to be in innate immunity, in which

  • SP-A binds to a variety of microorganisms,

  • promotes their clearance by phagocytic cells,

  • and directly alters the function of immune effector cells

Defense mechanisms and immunology

  • In humans, almost all the SP-A is found in the alveoli,

  • there is SP-A in human tracheal submucosal glands

  • low-level expression in some nonpulmonary tissues

Defense mechanisms and immunology

  • SP-A–deficient mice are more susceptible to infection by :

  • group B Streptococcus,

  • Pseudomonas aeruginosa,

  • Haemophilus influenza,

  • respiratory syncytial virus,

  • Pneumocystis carinii.



  • SP-A binds to and increases phagocytosisof Streptococcus pneumoniae, group A Streptococcus, and Staphylococcus aureus.

  • isolated SP-A binds to and increases the phagocytosis of H. influenzae, Klebsiella, and P. aeruginosa.

  • SP-A and SP-D could directly kill gram-negative bacteria by increasing their membrane permeability.

Mycobacteria fungi mycoplasma and pneumocystis

Mycobacteria, Fungi, Mycoplasma, and Pneumocystis.

  • SP-A enhances the adherence and subsequent phagocytosis of mycobacteria by macrophages.

  • SP-A bound to Aspergillus fumigatus conidia and enhanced their phagocytosis and killing by human neutrophils and alveolar macrophages.

  • SP-A could directly kill extracellular, but not intracellular, Histoplasma.

Defense mechanisms and immunology

  • SP-A appears to suppress the secretion of inflammatory cytokines by macrophages in the normal lung but enhances cytokine production during infection or lung injury.

    (inflammatory paradox of SP-A)

  • SP-A has also been shown to bind to apoptotic cells and to increase their uptake and removal by macrophages

Surfactant protein d

Surfactant Protein D

  • SP-D is a calcium-dependent lectin and an important component of innate immunity

  • The knockout mouse shows an accumulation of large foamy macrophages with excess metalloprotease activity  alveolar wall destruction and subsequent air space enlargement

  • susceptible to infection with influenza A virus and Aspergillus.

Defense mechanisms and immunology

  • annual severity of influenza infections is related to their ability to bind to SP-D : strains with less SP-D binding are more virulent.

Innate immunity in the lungs

Innate Immunity in the Lungs

Defense mechanisms and immunology

  • anatomic structure and epithelial cell lineages of the tracheobronchial tree

  • particles in excess of 10 µm in diameter are deposited on the mucus-coated surfaces of the nose, pharynx, trachea,descending airways



  • The classic antimicrobial defense mechanism in the conducting airways is the mucociliary system, which moves microbes deposited on the airway epithelial surface upward and out of the lungs

  • major antibacterial components include

  • lysozyme,

  • lactoferrin,

  • β-defensins



  • PMNs serve as the immediate effector arm of the innate immune system

  • the pulmonary capillaries slow the transit of PMNs because of the small cross-sectional capillary diameter.This produces a reservoir of capillary PMNs that are poised to respond directly to signals from the innate immune system in the air spaces.

Defense mechanisms and immunology

  • Once in the air spaces, PMNs ingest bacteria and fungi that have been opsonized by complement and immunoglobulins that accumulate in the air spaces at sites of inflammation.

  • PMNs contain a series of effector mechanisms to kill bacteria and fungi:

  • oxidant production,

  • microbicidal proteins in primary azurophilic granules,

  • extracellular traps.

Defense mechanisms and immunology

  • When defensins are added to the phagolysosomal space, they attach to negatively charged microbial membranes via electrostatic interactions and are thought to form lytic pores in the microbial cell wall.

  • at sites of intense inflammation, PMNs release superoxide anion, H2O2, and granular contents directly into the extracellular environment, leading to oxidant formation in the alveolar spaces

Defense mechanisms and immunology

  • PMNs can project uncoiled nuclear DNA into the surrounding environment to form NETs (neutrophil extracellular traps) that ensnare and destroy bacteria

  • NET formation depends on the initial respiratory burst of the PMN and leads to the death of the PMN in a process that is distinct from apoptosis and necrosis.

  • Login