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Old 06-02-2015
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Default Granuloma

Can anyone explain why macrophages release ACE and a-1 hydroxylase with granulomas?
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Quote:
Originally Posted by cma4_ View Post
Can anyone explain why macrophages release ACE and a-1 hydroxylase with granulomas?
Check mina's post (below)
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Last edited by CleverFOX; 06-03-2015 at 03:35 AM. Reason: I was wrong
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CleverFox,
Thanks for the reply, that makes sense. Now just have to figure out the ACE part.
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what happen with TB is called dystrophic calcification (mean deposition of ca in dead tissue not due to high serum ca level). the calcification from high ca is called metastatic calcification... TB granuloma has dystrophic calciification and it doesn't produce 1-a hydrolyase but sarcadosis granuloma has this enzyme and and ACE because it happen that sarcdosis most common in lung which make these enzymes normally in normal levels and some think that vitamin d has innate immune activity and we don't know causes of sarcadosis so i don't think we know why the body behave like this
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Quote:
Originally Posted by mina elisha View Post
what happen with TB is called dystrophic calcification (mean deposition of ca in dead tissue not due to high serum ca level). the calcification from high ca is called metastatic calcification... TB granuloma has dystrophic calciification and it doesn't produce 1-a hydrolyase but sarcadosis granuloma has this enzyme and and ACE because it happen that sarcdosis most common in lung which make these enzymes normally in normal levels and some think that vitamin d has innate immune activity and we don't know causes of sarcadosis so i don't think we know why the body behave like this
I think mina is correct I am editing my above post....I knew about the dystrophic calcification and non-caseating granulomas producing 1a-hydoxylase still took a guess I was wrong thanks for correcting me
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Mina,
Thanks for the response. I think what I was looking for it explained here. The ACE is released from damaged cells. Not produced in excess or any kind of response.

Chest. 1987 Jan;91(1):52-6.
Angiotensin converting enzyme in bronchoalveolar lavage in ARDS.
Idell S, Kueppers F, Lippmann M, Rosen H, Niederman M, Fein A.
Abstract

Angiotensin converting enzyme (ACE) is present in the endothelial cells of the normal lung where it converts angiotensin I to angiotensin II and inactivates bradykinin. It has been suggested that during endothelial injury ACE is sloughed into the blood, and that if the alveolar capillary membrane is injured, also into the alveolar lining fluid. Seven patients with adult respiratory distress syndrome (ARDS), were compared to 11 normal control subjects, nine patients with sarcoidosis, and six with idiopathic pulmonary fibrosis. Total, differential cell counts and ACE determinations were performed on bronchoalveolar lavage fluid in the ARDS group. ACE was detectable in the BAL of all but one ARDS patient. It was concluded that BAL ACE is elevated in some ARDS patients, especially those with infectious causes of lung injury. Increased ACE may reflect endothelial damage or local increase in ACE production in response to sepsis.
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"It was concluded that BAL ACE is elevated in some ARDS patients, especially those with infectious causes of lung injury"
i agree it will increase big time because of the direct damage in alveloar-caplliary interface. but also increase production as response for this inflammation-mediated damage to inactivate the bradykinin which is one of the inflammatory mediators...i think
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