Pathology
Immune Responses
Which of the following complement proteins are the main chemoattractants for recruiting inflammatory cells:
Answer:
The complement pathway generates the biologically active fragments C3a and C5a which are chemoattractant for neutrophils and monocytes and which stimulate degranulation of mast cells and basophils.Complement Cascade
Pathology / Immune Responses
Last Updated: 13th April 2023
This consists of a series of plasma proteins constituting an amplification enzyme system which is capable of lysis of bacteria/blood cells or opsonisation of bacteria/cells for phagocytosis. The complement sequence consists of nine major components, which are activated in turn and form a cascade, resembling the coagulation sequence. The most abundant and pivotal protein is C3.
Opsonisation
Macrophages and neutrophils have C3b receptors and they phagocytose C3b-coated cells. C3 deficiency thus leads to increased susceptibility of infection with encapsulated organisms (e.g. S. pneumoniae, H. influenzae).
The early stages leading to coating of the cells with C3b can occur by two different pathways:
- The classical pathway usually activated by IgG or IgM coating of cells
- The alternative pathway which is more rapid and activated by IgA, endotoxin and other factors
Membrane Attack Complex
If the complement sequence goes to completion, there is generation of an active phospholipase (the membrane attack complex, MAC) that punches holes in the cell membrane causing cell lysis. The MAC appears to be the only way of killing the Neisseria family of bacteria and thus C5 - C9 deficiency results in increased susceptibility to Neisseria infections.
Anaphylactoids
The complement pathway also generates the biologically active fragments C3a and C5a which are chemoattractant for neutrophils and monocytes and which stimulate degranulation of mast cells and basophils.
Regulation
The complement pathway is regulated by complement inhibitors e.g. decay accelerating factor or C1 inhibitor. Deficiency in C1 inhibitor results in hereditary angioedema. Deficiency in complement decay-accelerating factor results in paroxysmal nocturnal haemoglobinuria.
Complement Cascade. (Image by OpenStax College [CC BY 3.0 (https://creativecommons.org/licenses/by/3.0)])
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- Biochemistry
- Blood Gases
- Haematology
| Biochemistry | Normal Value |
|---|---|
| Sodium | 135 – 145 mmol/l |
| Potassium | 3.0 – 4.5 mmol/l |
| Urea | 2.5 – 7.5 mmol/l |
| Glucose | 3.5 – 5.0 mmol/l |
| Creatinine | 35 – 135 μmol/l |
| Alanine Aminotransferase (ALT) | 5 – 35 U/l |
| Gamma-glutamyl Transferase (GGT) | < 65 U/l |
| Alkaline Phosphatase (ALP) | 30 – 135 U/l |
| Aspartate Aminotransferase (AST) | < 40 U/l |
| Total Protein | 60 – 80 g/l |
| Albumin | 35 – 50 g/l |
| Globulin | 2.4 – 3.5 g/dl |
| Amylase | < 70 U/l |
| Total Bilirubin | 3 – 17 μmol/l |
| Calcium | 2.1 – 2.5 mmol/l |
| Chloride | 95 – 105 mmol/l |
| Phosphate | 0.8 – 1.4 mmol/l |
| Haematology | Normal Value |
|---|---|
| Haemoglobin | 11.5 – 16.6 g/dl |
| White Blood Cells | 4.0 – 11.0 x 109/l |
| Platelets | 150 – 450 x 109/l |
| MCV | 80 – 96 fl |
| MCHC | 32 – 36 g/dl |
| Neutrophils | 2.0 – 7.5 x 109/l |
| Lymphocytes | 1.5 – 4.0 x 109/l |
| Monocytes | 0.3 – 1.0 x 109/l |
| Eosinophils | 0.1 – 0.5 x 109/l |
| Basophils | < 0.2 x 109/l |
| Reticulocytes | < 2% |
| Haematocrit | 0.35 – 0.49 |
| Red Cell Distribution Width | 11 – 15% |
| Blood Gases | Normal Value |
|---|---|
| pH | 7.35 – 7.45 |
| pO2 | 11 – 14 kPa |
| pCO2 | 4.5 – 6.0 kPa |
| Base Excess | -2 – +2 mmol/l |
| Bicarbonate | 24 – 30 mmol/l |
| Lactate | < 2 mmol/l |
