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We often hear about how bad antibiotics are for us. That's why I found it very interesting to read about the many positive effects antibiotics can have, besides destroying bacteria.
http://www.aldf.com/Book_Review_on_Antibiotics_as_inflamatory_agents.pdf
Abilities (1) to suppress the expression of virulence factors (e.g., quorum sensing mechanisms, as well as the production of exotoxins, exopolysaccharides, pili, flagellin, and lipopolysaccharides);
(2) to accumulate in in-flammatory cells in high concentration, thereby providing more efficient deliveryof antibiotic to sites of infection;
(3) to downregulate the molecular expression of integrins known to influence leukocyte
adhesion and the accumulation of macrophages and neutrophils at sites of infection; (4) to inhibit the maturation and proliferation of subsets of T lymphocytes,
as well as to influence immunoglobulin secretion and isotype class switching by B
lymphocytes;
(5) to protect the respiratoryciliated epithelium from bacterial injury
by interfering with bacterial adherenceand colonization;
(6) to inhibit neutrophil migration;
(7) to modulate the expression of adhesion molecules and to reduce the
production of chemotactic factors at the site of inflammation;
(8) to increase the
production of various inflammatory cytokines (IL-8, IL-1b, and TNF-a) that are
potent activators of neutrophils;
(9) to increase the production of IL-2, colony stimulating factor, and other cytokines that modulate the induction of TH1 and TH2
lymphocyte activity; and
(10) to cause significant reductions in the number of lymphocytes and the ratio of CD4+CD8+T lymphocytes.
The clinical implications of some of these effects are discussed with reference
to which antibiotics are used as mucoregulatory agents for treating diffuse panbronchiolitis, cystic fibrosis, various upper airway diseases, chronic asthma, and lung injury, as well as which antibiotics are used for the development of more precise therapies to prevent biofilm diseases or chronic inflammation without increasing
the risk of antimicrobial resistance to macrolides. The implications of these findings
with respect to protracted antibiotic therapy remain to be fully assessed. If one also
considers the results of a recent study [1] that indicates that as many as 15 different
b-lactam antibiotics, including penicillin and its derivatives, exert profound neuroprotective effects, it, indeed, may be difficult at times to attribute the beneficial
effects antibiotic therapy to any particular mechanism.
http://jpet.aspetjournals.org/content/292/1/156.full
In conclusion, the present study shows that macrolide antibiotics have anti-inflammatory activity, which likely depends on their ability to prevent the production of proinflammatory mediators and cytokines, and suggests that these agents, particularly roxithromycin, can exert therapeutic effects independent of their antibacterial activity.
http://www.aldf.com/Book_Review_on_Antibiotics_as_inflamatory_agents.pdf
Abilities (1) to suppress the expression of virulence factors (e.g., quorum sensing mechanisms, as well as the production of exotoxins, exopolysaccharides, pili, flagellin, and lipopolysaccharides);
(2) to accumulate in in-flammatory cells in high concentration, thereby providing more efficient deliveryof antibiotic to sites of infection;
(3) to downregulate the molecular expression of integrins known to influence leukocyte
adhesion and the accumulation of macrophages and neutrophils at sites of infection; (4) to inhibit the maturation and proliferation of subsets of T lymphocytes,
as well as to influence immunoglobulin secretion and isotype class switching by B
lymphocytes;
(5) to protect the respiratoryciliated epithelium from bacterial injury
by interfering with bacterial adherenceand colonization;
(6) to inhibit neutrophil migration;
(7) to modulate the expression of adhesion molecules and to reduce the
production of chemotactic factors at the site of inflammation;
(8) to increase the
production of various inflammatory cytokines (IL-8, IL-1b, and TNF-a) that are
potent activators of neutrophils;
(9) to increase the production of IL-2, colony stimulating factor, and other cytokines that modulate the induction of TH1 and TH2
lymphocyte activity; and
(10) to cause significant reductions in the number of lymphocytes and the ratio of CD4+CD8+T lymphocytes.
The clinical implications of some of these effects are discussed with reference
to which antibiotics are used as mucoregulatory agents for treating diffuse panbronchiolitis, cystic fibrosis, various upper airway diseases, chronic asthma, and lung injury, as well as which antibiotics are used for the development of more precise therapies to prevent biofilm diseases or chronic inflammation without increasing
the risk of antimicrobial resistance to macrolides. The implications of these findings
with respect to protracted antibiotic therapy remain to be fully assessed. If one also
considers the results of a recent study [1] that indicates that as many as 15 different
b-lactam antibiotics, including penicillin and its derivatives, exert profound neuroprotective effects, it, indeed, may be difficult at times to attribute the beneficial
effects antibiotic therapy to any particular mechanism.
http://jpet.aspetjournals.org/content/292/1/156.full
In conclusion, the present study shows that macrolide antibiotics have anti-inflammatory activity, which likely depends on their ability to prevent the production of proinflammatory mediators and cytokines, and suggests that these agents, particularly roxithromycin, can exert therapeutic effects independent of their antibacterial activity.
